Alteration in the Female Reproductive System Flashcards
Complete androgen insensitivity syndrome
characterized by external female genitalia
children with CAIS often have testes within the labia majora, inguinal ring, or abdominal cavity that produce testosterone (and estrogen) in normal-range levels.
Breast development may be normal, but pubic and axillary hair is often sparse and the cervix, uterus, and ovaries are absent. A short vagina that ends without a cervix also may be present.
These individuals are often undiagnosed until puberty when menarche does not occur.
partial androgen insensitivity syndrome (PAIS)
ambiguous genitalia and varying genotype
Treatment for Complete Androgen Insensitivity Syndrome (CAIS)
Gonadectomy and hormone replacement therapy
normal range for the onset of puberty
8 to 13 years
Delayed puberty is diagnosed if
there is no breast development by age 13
the absence of a period by age 15 or 16.
functional hypogonadotropic hypogonadism
underlying condition or illness (unrelated to gonadal function) responsible for the delayed development of puberty
treated with hormone therapy
Precocious puberty
the onset of clinical signs of puberty (breast or pubic hair development) before age 8.
Results of precocious puberty
premature development of secondary sex characteristics
premature closure of the epiphysis of long bones, which results in lifelong short stature
often carries profound psychosocial consequences
Causes of precocious puberty
alterations in genetic factors,
an increase in obesity,
an increase in protein consumption,
the growing prevalence of molecular compounds known as endocrine disruptors in common household products
Central precocious puberty
results from failure of central inhibition of the GnRH pulse generator (the gonadostat), often because of CNS abnormality
Partial precocious puberty
partial early development of appropriate secondary sex characteristics alone or in combination
develop breasts and pubic hair early
Complete precocious puberty
onset and progression of all pubertal features
Primary dysmenorrhea
painful menstruation associated with the release of prostaglandins in ovulatory cycles,
secondary dysmenorrhea
related to pelvic pathologic disorders (i.e., ovarian cysts, adenomyosis, endometriosis) that manifest in later reproductive years and may occur any time in the menstrual cycle
Causes of primary dysmenorrhea
Elevated levels of prostaglandins (especially PGF2α and PGE2α) cause uterine hypercontractility, decreased blood flow to the uterus, and increased nerve hypersensitivity, resulting in pain.
chief symptom of dysmenorrhea
pelvic pain associated with the onset of menses
pain often radiates into the groin and may be accompanied by backache, anorexia, vomiting, diarrhea, syncope, insomnia, and headache
dysmenorrhea symptoms are caused by
entry of prostaglandins and prostaglandin metabolites into the systemic circulation
treatment of dysmenorrhea
nonsteroidal anti-inflammatory drugs (reduce COX enzyme activity, and thus prostaglandin production)
hormonal contraceptives (stops ovulation and creates an atrophic endometrium, thereby decreasing prostaglandin synthesis and myometrial contractility)
Amenorrhea
Lack of menstruation,
causes of amenorrhea
pregnancy
chromosomal abnormalities,
hypothalamic dysfunction,
polycystic ovarian syndrome, hyperprolactinemia,
hypothyroidism,
malnutrition
ovarian failure
Primary amenorrhea
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
Compartment IV disorders
hypothalamus is unable to synthesize GnRH, so the pituitary fails to secrete LH and FSH. Therefore the ovary does not receive the hormonal signals required to stimulate estrogen production, and ovulation and menstruation do not occur
Compartment II disorders
involve the ovary and are often linked with genetic abnormalities
gonadal dysgenesis (Turner syndrome) or androgen insensitivity syndrome (AIS)
Compartment III disorders
disorders of the anterior pituitary gland including tumors
interfere with, or interrupt, the secretion of GnRH or FSH and LH
hydrocephalus, craniopharyngiomas, and other space-occupying lesions of the CNS
Compartment I disorders
anatomic defects of the outflow tract associated with primary amenorrhea
congenital absence of the vagina and uterus and congenital uterine hypoplasia
Turner syndrome
involves the lack of two functional and complete X chromosomes in at least some body tissues
failure of secondary sex characteristic development and amenorrhea, although there are high levels of circulating FSH and LH
androgen insensitivity syndrome (AIS)
cells do not have a receptor for testosterone
patient have female external genitalia and female secondary sex characteristics. With the exception of a small vagina, internal female genitalia are absent, accounting for amenorrhea and infertility
Typical primary dysmenorrhea sufferers are:
younger than 30
have not given birth
have a history of pelvic inflammatory disease, sexual assault, premenstrual syndrome, or sterilization;
are heavy tobacco or alcohol users
have a family history of dysmenorrhea
have a body mass index (BMI) less than 20
Diagnosis of amenorrhea
Absence of sexual characteristics
the appearance of an immature female
structural or physiologic alterations of the reproductive tract
Laboratory studies to document karyotype, abnormal levels of gonadotropins, thyroid and prolactin levels, and ovarian hormones
Secondary amenorrhea
absence of regular menses for 3 months or irregular menses for 6 months in women who have previously menstruated
Causes of secondary amenorrhea
pregnancy
thyroid disorders (e.g., hypothyroidism), hyperprolactinemia
HPO interruption secondary to excessive exercise,
stress,
weight loss,
polycystic ovary syndrome (PCOS)
major manifestations of secondary amenorrhea
absence of menses after previous menstrual periods. Infertility
vasomotor flushes
vaginal atrophy
acne
osteopenia
hirsutism
