Class notes
Nu 545 Unit 3 study guide
- Course
- NU 545
- Institution
- University Of South Alabama
This is a comprehensive and detailed study guide for unit 8, it includes 8 key chapters in Nu 545.
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Unit 3 Study Guide NU 5451.Know all STIS: pathophysiology, etiology, clinical manifestations, diagnostic tests, treatment, and complications.
P.869
What organism causes each STI and is it viral, bacterial etc.?
How is each transmitted during pregnancy to the fetus?
STIs also can be transmitted from mother to child during pregnancy and birth, a process known as vertical
transmission.
Know the different stages of syphilis
Primary syphilis
begins at the site of bacterial invasion, where T. pallidum multiplies in the epithelium and produces a
granulomatous tissue reaction called a chancre.
Some microorganisms drain with lymph into adjacent lymph nodes.
Within the nodes and at the site of the chancre, the cell-mediated and humoral immune responses are stimulated.
Secondary syphilis
is systemic.
During this stage, blood-borne bacteria spread to all major organ systems.
The secondary stage is followed by a period during which the immune system is able to suppress the
infection.
Even without treatment, spontaneous resolution of the skin lesions occurs and the individual enters the latent stage
of infection.
Latent syphilis
may be subdivided into early and late stages; however, no specific criteria delineate one from the other.
Medical history and serologic studies can show that syphilis is present, but the individual has no clinical
manifestations.
Transmission remains possible during this phase.
Tertiary syphilis
is the most severe stage, involving significant morbidity and mortality.
The pathogenesis of syphilitic manifestations at this stage remains unclear.
The destructive skin, bone, and soft tissue lesions (called gummas) of tertiary syphilis probably are caused by a
severe hypersensitivity reaction to the microorganism.
Within the cardiovascular system, infection with T. pallidum may cause aneurysms, heart valve insufficiencies, and
heart failure.
Do you treat both partners and why?
Allowing doctors to treat both patients and their partners in this way has proven to be effective at preventing
reinfection and the spread of infections such as chlamydia and gonorrhea.
Long term, there are many societal benefits both in health and cost.
1
, Treatment of the person and his or her sexual partner(s) is often complicated by inadequate access to medical care, drug
cost, and privacy concerns.
Many states have enacted legislation to allow sexual partners to be treated without having to go to a clinic for an
examination and prescription.
What age group has the greatest risk of STIs and why?
Young people ages 15-24
rates of gonorrhea, chlamydia, vaginitis, cervical condyloma, genital warts, and pelvic inflammatory disease (PID) are
highest in adolescents and decline exponentially with increasing age.
Adolescents more often engage in risky behaviors and have a greater number of sexual partners than older adults. \
What causes cervical cancer?
HPV
2.Understand the different uterine tumor types.
Endometrial polyp
is a benign mass of endometrial tissue, covered by a surface epithelium, and contains a variable amount of glands, stroma, and blood vessels.
Endometrial polyps can occur anywhere within the uterus.
Polyps are morphologically diverse and usually classified as hyperplastic, atrophic (or inactive), or functional.
In the last case, the surface epithelium may be “out of phase” with other endometrial tissue.
Hyperplastic polyps are often pedunculated and may be mistaken for endometrial hyperplasia or, if large, adenosarcoma.
Although polyps most often develop in women between ages 40 and 50, they can occur at all ages.
These are often related to estrogen stimulation. An estimated 20% to 25% of women have uterine polyps, including as many as 35% of women with
abnormal uterine bleeding.
Endometrial polyps are a common cause of intermenstrual or excessive menstrual bleeding.
Diagnosis is made by transvaginal sonography or hysteroscopy.
Risk factors include advanced age; obesity; nulliparity; early menarche or late menopause, or both; diabetes; tamoxifen use; hypertension; and estrogenic
states (i.e., anovulatory cycles and unopposed estrogen).
Malignancy is rare (up to 4.8% of polyps have evidence of malignancy); however, polyps that cause abnormal bleeding have twice the rate of malignancy
of asymptomatic polyps.
Coexistence of a separate endometrial atypical hyperplasia or adenocarcinoma is common.
Uterine polyps have a high rate of spontaneous resolution but have been associated with suboptimal fertility.
Polypectomy can be performed through hysteroscopy for symptomatic women, for those at risk for malignancy, or for women who are struggling to
conceive.
Leiomyomas
commonly called myomas or uterine fibroids, are benign smooth muscle tumors in the myometrium
Leiomyomas are the most common benign tumors of the uterus, affecting as many as 70% to 80% of all women, and most remain small,
asymptomatic, and clinically insignificant.
Prevalence increases in women ages 30 to 50 but decreases with menopause.
The incidence of leiomyomas in black and Asian women is two to five times higher than that in white women, and the age of onset for black women is,
on average, 10 years earlier than that for white women.
Complications related to leiomyomas are the primary reason for gynecologic hospitalizations and account for 30% of all hysterectomies in women less
than 40 years of age.
The cause of uterine leiomyomas is unknown, although their size appears to be related to estrogen, progesterone, growth factors, angiogenesis,
and apoptosis.
There is a genetic component to fibroids, and the leiomyomas exhibit chromosomal changes within their tissues.
Leiomyomas are estrogen- and progesterone-sensitive and are found to have increased numbers of estrogen receptors.
Uterine leiomyomas are not seen before menarche, and those that develop during the reproductive years generally decrease in size after menopause.
Occurrence is multifactorial but often linked with estrogen exposure.
Tumors in pregnant women may enlarge rapidly but often decrease in size after the end of the pregnancy.
Risk factors for fibroids include nulliparity, obesity, PCOS, black race, postmenopausal hormone use, and hypertension.
3.What is PCOS and what does it cause? Clinical manifestations? Treatment? Causes? Pathophysiology?
4.What is the difference between primary and secondary amenorrhea and what is compartment II?
Polycystic ovary syndrome (PCOS)
is the most common cause of anovulation and ovulatory dysfunction in women.
At least two of the following three features: irregular ovulation, elevated levels of androgens (e.g., testosterone),
and the appearance of polycystic ovaries on ultrasound.
o Polycystic ovaries do not have to be present to diagnose PCOS, and conversely their presence alone does not establish the diagnosis.
The diagnosis is one of exclusion, and all other disorders potentially responsible for the clinical findings also must be
ruled out, including thyroid dysfunction, hyperprolactinemia, and congenital adrenal hyperplasia.
PCOS is associated with metabolic dysfunction, including dyslipidemia, insulin resistance, and obesity.
There is a strong genetic component to PCOS, and various features of the syndrome may be differentially inherited.
Signs and symptoms of women with PCOS may change over time, with metabolic syndrome becoming more prominent
with age.
polycystic ovaries may be associated with Cushing syndrome, acromegaly, premature ovarian failure, simple obesity,
congenital adrenal hyperplasia, thyroid disease, androgen-producing adrenal tumors or ovarian tumors and syndromes
with hyperprolactinemia
Pathophysiology
Although the underlying cause of PCOS is unknown, a genetic basis is suspected.
2
, o Initial identification of genes involved in steroid biosynthesis, androgen biosynthesis, and insulin receptors within the ovary indicates genetic
involvement.
o No single factor fully accounts for the abnormalities of PCOS.
A hyperandrogenic state is a cardinal feature in the pathogenesis of PCOS.
However, glucose intolerance/insulin resistance (IR) and hyperinsulinemia often run parallel to and markedly
aggravate the hyperandrogenic state, thus contributing to the severity of signs and symptoms of PCOS.
Women with PCOS are three times as likely to have insulin resistance.
Insulin stimulates androgen secretion by the ovarian stroma and reduces serum sex hormone–binding globulin (SHBG)
directly and independently. The net effect is an increase in free testosterone levels.
Excessive androgens affect follicular growth, and insulin affects follicular decline by suppressing apoptosis and
enabling follicles to persist.
genetic ovarian defect in PCOS, which makes the ovary either more susceptible to or sensitive to insulin's stimulation
of androgen production.
Recent research suggests that decreased intraovarian receptors for estrogen receptor-α or insulin-like growth
factor 1 (IGF-1), increased leptin levels, or direct infrared radiation within selective ovarian cells (fibroblasts)
may contribute to this phenomenon.
Intrauterine and early childhood environments may also contribute to the development of PCOS
Weight gain tends to aggravate symptoms, whereas weight loss may ameliorate some of the endocrine and
metabolic events and thus decrease symptoms.
Women with PCOS tend to have increased leptin levels (leptin levels are increased in thin as well as overweight
women with PCOS).
Leptin influences the hypothalamic pulsatility of GnRH and consequent interaction along the entire HPO axis.
Feedback from the polycystic ovary is disturbed because of changes in ovarian steroid and nonsteroidal (inhibins and
related proteins) hormones.
In PCOS there is dysfunction in ovarian follicle development.
Inappropriate gonadotropin secretion triggers the beginning of a vicious cycle that perpetuates anovulation. Typically,
levels of FSH are low or below normal and LH levels and LH bioactivity are elevated.
An increased frequency of GnRH pulses appears to cause increased frequency of LH pulses.
Persistent LH elevation causes an increase in the levels of androgens (dehydroepiandrosterone sulfate [DHEAS] from
the adrenal glands and testosterone, androstenedione, and DHEAS from the ovary).
Androgens are converted to estrogen in peripheral tissues, and increased testosterone levels cause a significant
reduction (approximately 50%) in SHBG, which in turn causes increased levels of free estradiol. Elevated estrogen
levels trigger a positive-feedback response in LH and a negative-feedback response in FSH.
Because FSH levels are not totally depressed, new follicular growth is continuously stimulated, but not to full
maturation and ovulation.
The accumulation of follicular tissue in various stages of development allows an increased and relatively constant
production of steroids in response to gonadotropin stimulation.
Thus PCOS is characterized by excessive production of both androgen and estrogen.
Increased androgen secretion by the ovaries contributes to premature follicular failure (atresia) and persistent
anovulation.
persistent anovulation causes enlarged polycystic ovaries characterized by a smooth, pearly white capsule.
This characteristic appearance is caused by an increase of surface area and increased volume of up to 2.8 times,
doubling of growing and atretic follicles, thickening of the tunica (outermost area) by 50%, increasing cortical stromal
thickening by one-third and a fivefold increase in subcortical stroma, and escalating hyperplasia.
With advancing age, menstrual irregularities may improve while the incidence of metabolic syndrome and type 2
diabetes mellitus increases.
Women with PCOS have a three times greater incidence of uterine cancer in later life than normally cycling
women related to the anovulatory lack of progesterone in PCOS.
Without treatment for anovulation, women with PCOS have a 9% lifetime risk for endometrial cancers related to the
effects of unopposed estrogen.
Clinical Manifestations
usually appear within 2 years of puberty but may present after a variable period of normal menstrual function and,
possibly, pregnancy.
The symptoms are related to anovulation, hyperandrogenism, and insulin resistance and include dysfunctional
bleeding or amenorrhea, hirsutism, acne, acanthosis nigricans, and infertility.
Approximately 60% of women with PCOS are obese.
are more likely to experience sleep apnea than unaffected women, which results in impaired sleep and may reduc their
overall quality of life.
Evaluation
Diagnosis of PCOS is based on evidence of androgen excess, chronic anovulation, and sonographic evidence of
polycystic ovaries with at least two of the three criteria present.
Tests for impaired glucose tolerance are recommended.
3
, polycystic ovaries do not have to be present and, conversely, their presence alone does not establish the
diagnosis.
Because of the normalcy of anovulatory cycles in adolescence, evidence of hyperandrogenism (in the setting of
irregular menses) must be present before PCOS is diagnosed in an adolescent female.
Treatment
reversing signs and symptoms of androgen excess, instituting cyclic menstruation, restoring fertility, and
ameliorating any associated metabolic or endocrine, or both, disturbances.
First-line treatment of PCOS includes combined oral contraceptives (COCs) for management of symptoms (e.g.,
hirsutism, acne) and to establish regular menses.
For those women with PCOS who are overweight or obese, lifestyle modifications, including regular exercise and
weight loss, also are considered first-line treatments.
Women with insulin resistance, or those women who do not respond to contraceptive therapy, may benefit from the
insulin sensitizer metformin.
If COCs are not used and pregnancy is not desired, progesterone therapy is recommended to oppose estrogen's
effects on the endometrium and as a means to initiate monthly withdrawal bleeding (at the expense of continued
hirsutism).
For overweight or obese infertile women desiring pregnancy, lifestyle modifications are first-line therapy.
Even a small reduction of weight restores ovulation and increases insulin sensitivity by 71% in obese women with
PCOS. Reduction of insulin by loss of abdominal fat appears crucial in restoring ovulation.
Clomiphene citrate, an antiestrogen, can be used to facilitate ovulation and can be combined with metformin for
improved outcomes.
Management of PCOS is a nearly lifelong process because the effects of the syndrome persist past childbearing years.
Appropriate primary care is needed to control the systemic features of PCOS so that it has minimal impact on a
woman's life and health outcomes.
Primary amenorrhea
is the failure of menarche and the absence of menstruation by age 13 years, without the development of
secondary sex characteristics, or by age 15 regardless of the presence of secondary sex characteristics.
Secondary amenorrhea
is the absence of regular menses for 3 months or irregular menses for 6 months in women who have previously
menstruated. Pregnancy is the most common condition to exclude before further evaluation.
Compartment III disorders
are disorders of the anterior pituitary gland including tumors.
Some anatomic defects of the CNS, whether congenital or acquired, impinge on the hypothalamic-pituitary unit so as to interfere with, or
interrupt, the secretion of GnRH or FSH and LH.
Examples of such defects include hydrocephalus, craniopharyngiomas, and other space-occupying lesions of the CNS.
The target organ, the ovary, does not receive the necessary signals and ovulation and menstruation do not occur.
In some cases, these lesions develop between the onset and conclusion of puberty.
o Therefore skeletal growth may occur and secondary sex characteristics may develop, but sexual maturation is interrupted before menarche.
Autoimmune disease, hyperprolactinemia, and some medications also can affect the pituitary and disrupt normal menstruation.
Compartment II disorders
involve the ovary and are often linked with genetic abnormalities.
These include gonadal dysgenesis (Turner syndrome) or androgen insensitivity syndrome (AIS)
Turner syndrome involves the lack of two functional and complete X chromosomes in at least some body tissues
(45,X/46,XX; structural X or Y abnormalities; mosaicism), which results in the ovaries lacking gametes and ovarian
failure.
Without primitive gametes and follicles, follicular development and estrogen secretion cannot occur.
Lack of estrogen accounts for failure of secondary sex characteristic development and amenorrhea, although there are
high levels of circulating FSH and LH.
5.What are the signs of puberty in girls and boys? What delays puberty?
Girls
puberty begins at about ages 8 to 9 years with thelarche (breast development).
Estradiol causes development of the breasts (thelarche), maturation of the reproductive organs (vagina, uterus,
ovaries), and deposition of fat deposits in the hips of girls.
In females, the ovaries begin to release mature ova.
Female puberty is complete with the first ovulatory menstrual period; however, this can take up to 1 to 2 years
after menarche.
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