Reproductive:
endometrial cycle and the occurrence of ovulation- the menstrual cycle consist of
three phases: the follicular/proliferative phase (postmenstrual), followed by the
luteal/secretory phase (premenstrual), and the ischemic/menstrual phase.
*Ovarian hormones control the uterine (endometrial) events of the menstrual
cycle. During the follicular/proliferative phase of the ovarian cycle estrogen
produced by the follicle causes the endometrium to proliferate (proliferative
phase) and induces the LH surge and progesterone production in the granulosa
layer. During the luteal/secretory phase, estrogen maintains the thickened
endometrium, and progesterone causes it to develop blood vessels and secretory
glands (secretory phase). As the corpus luteum “starved” endometrium
degenerates and sloughs off, causing menstruation, the ischemic/menstrual
phase.
uterine prolapse- the descent of the cervix or entire uterus into the vaginal canal
due to weakened pelvic fascia and musculature and poor support from the
vaginal muscles and fascia.
polycystic ovarian syndrome- most common cause of anovulation and ovulatory
dysfunction in women. Defined as having 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. PCOS is associated with
metabolic dysfunction, including dyslipidemia, insulin resistance, and obesity.
One of the most common endocrine disturbances affecting women, especially
young women, and is a leading cause of infertility in the U.S. Strong genetic
component to PCOS, various features of the syndrome may be inherited. PCOS
patients are three times as likely to have insulin resistance, higher for obese
women. Tend to have increased leptin levels. Symptoms within 2 years of puberty
& include: dysfunctional bleeding or amenorrhea, hirsutism, acne, acanthosis
nigricans, and infertility. 60% are obese. Increased risk for gestational DM,
pregnancy-induced HTN, preterm birth, and perinatal mortality.
testicular cancer and conditions that increase risk- most common cancer in men,
age 15-35. Slightly more common on the right than on the left. 90% of testicular
cancers are germ cell tumors arising from the male gametes. Two types:
Seminomas-most common, least aggressive, make up 30-35% of testicular
cancers & Nonseminomas-include embryonal carcinomas, teratomas, and
choriocarcinomas, which are the most aggressive, but rare form of testicular
cancer. Risk factors include: genetic predisposition, history of cryptorchidism,
abnormal testicular development, HIV, AIDS, Klinefelter syndrome, and history of
testicular cancer. Can arise from specialized cells of the gonadal stroma-these
tumors, which are named for their cellular origins, are Leydig cell, Sertoli cell,
granulosa cell, and theca cell tumors and constitute less than 10% of all testicular
cancers.
symptoms that require evaluation for breast cancer- painless lump, palpable
nodes in the axilla, retraction of tissue (dimpling), chest pain, dilated blood
,vessels, edema, edema of the arm, hemorrhage, local pain, nipple/areolar eczema,
nipple discharge in non-lacting woman, pitting of the skin (like surface of an
orange peel), reddened skin, local tenderness and warmth, skin retraction,
ulceration.
signs of premenstrual dysphoric disorder- One of these symptoms must be
present for a diagnosis: marked affective lability, marked irritability or anger or
increased interpersonal conflicts, marked anxiety, tension. One of these must
also be present: decreased interest, difficulty concentrating, easy fatigability, low
energy, increase or decrease in sleep, feelings of being overwhelmed, physical
symptoms, such as: breast tenderness, muscle or joint aches, bloating or weight
gain. (Greater than 5 of these symptoms occur during the week before menses
onset, improve within a few days after menses onset, and diminish in the week
postmenses).
dysfunctional uterine bleeding- bleeding that is abnormal in duration, volume,
frequency, or regularity; and has been present for the majority of the previous 6
months. May be acute or chronic. PALM-COEIN System for classification of
abnormal uterine bleeding: PALM-structural causes: Polyp, Adenomyosis,
Leiomyoma, Malignancy. COEIN-nonstructural causes: coagulopathy, ovulatory
dysfunction, endometrial, iatrogenic, not yet classified. Increased endometrial
bleeding is correlated with a change from ovulatory to anovulatory cycles due to
high estrogen levels.
pathophysiology of prostate cancer- More than 95% of prostatic neoplasms are
histologically similar to adenocarcinomas and rely on androgen-dependent
signaling for their development and progression. Most of these neoplasms occur
in the periphery of the prostate. Prostatic adenocarcinoma is a heterogeneous
group of tumors with a diverse spectrum of molecular and pathologic
characteristics, and therefore clinical behaviors and challenges. The biologic
aggressiveness of the neoplasm appears to be related to the degree of
differentiation rather than the size of the tumor. Testicular testosterone provides
the main source of androgens in the prostate and is the major circulating
androgen, whereas DHT predominates in prostate tissue and binds to the
androgen receptors with greater affinity than does testosterone. Androgen
production outside of the testes, or extra testicular sources. Testosterone is
converted to dihydrotestosterone, DHT is the most potent intraprostatic
androgen.
HPV and the development of cervical cancer- almost exclusively caused by
cervical human papillomavirus (HPV) infection. HPV strains 16 & 18 are most
often implicated as causing 70% of all cervical cancers and also contribute to
many vaginal, vulvar, penile, anal, and oropharyngeal cancers. Most HPV
infections are cleared from the immune system; vast majority of infections do not
cause cervical cancer. Screening before age 21 not recommended. Women with
multiple sex partners are more likely to be exposed to high-risk HPV, but women
with only one lifetime sexual partner can also become infected. Transformation
zone is where the two cell types of squamous epithelium cells and columnar
, epithelial cells come together and this is where carcinoma in situ is most likely to
develop. PAP test or HPV screening necessary for early detection; 90% can be
detected by these. Viral DNA becomes integrated into the genomic DNA of the
infected basal cell of the cervix and directs the persistent production of viral
oncogenes. Persistence of infection with high-risk HPV is a prerequisite for the
development of cervical intraepithelial neoplasia, lesions, and invasive cervical
cancers.
Endocrine:
body’s process for adapting to high hormone levels- Feedback systems. Most
hormone levels are regulated by negative feedback, in which tropic hormone
secretion raises the level of a specific hormone. The elevated level of the specific
hormone then causes negative feedback, decreasing secretion of the tropic
hormone. Positive feedback systems, in which elevated hormone levels increase
a response which then further increases hormone secretion, is seen most often in
reproductive hormones. Negative feedback is the most common & occurs when a
chemical, neural, or endocrine response decreases the subsequent synthesis and
secretion of a hormone. Positive feedback occurs when a neural, chemical, or
endocrine response increases the synthesis and secretion of a hormone. Positive
feedback also occurs when an increased hormone level further increases the
synthesis and secretion of that same hormone. The sensitivity or affinity of the
target cell to a particular hormone is related to the concentration of receptors per
cell: the more receptors, the higher the affinity or the more sensitive the cell is to
the stimulating effects of the hormone. Thus the cell can adjust its sensitivity to
the concentration of the signaling hormone. hormone is distributed throughout
the body, only target cells with specific receptors for that hormone are affected.
Target cell response depends on blood levels of the hormone, the concentration
of target cell receptors, and affinity of the receptor for the hormone. Hormone
receptors of the target cell have two main functions: (1) to recognize and bind
with high affinity to their particular hormones and (2) to initiate a signal to
appropriate intracellular effectors. See Chapter 1 for cell signaling pathways,
particularly.
Cushing’s Syndrome- the clinical manifestations resulting from chronic exposure
to excess endogenous cortisol and is more common in women. Cushing’s
disease is excess endogenous secretion of ACTH. ACTH dependent
hypercortisolism (about 80%) results from overproduction of pituitary ACTH by a
pituitary adenoma (most common and can occur at any age) or by an ectopic
secreting nonpituitary tumor, such as a small cell carcinoma of the lung (more
common in older adults). ACTH-independent hypercortisolism (about 20%) is
caused by cortisol secretion from a rare benign or malignant tumor of one or both
adrenal glands (more common in children). A Cushing-like syndrome may
develop as a side effect of long-term pharmacologic administration of
glucocorticoids. With ACTH-dependent hypercortisolism, the excess ACTH
stimulates excess production of cortisol and there is loss of feedback control of
ACTH secretion. Whatever the cause, two observations consistently apply to
individuals with Cushing’s syndrome: 1.) They don’t have diurnal or circadian
endometrial cycle and the occurrence of ovulation- the menstrual cycle consist of
three phases: the follicular/proliferative phase (postmenstrual), followed by the
luteal/secretory phase (premenstrual), and the ischemic/menstrual phase.
*Ovarian hormones control the uterine (endometrial) events of the menstrual
cycle. During the follicular/proliferative phase of the ovarian cycle estrogen
produced by the follicle causes the endometrium to proliferate (proliferative
phase) and induces the LH surge and progesterone production in the granulosa
layer. During the luteal/secretory phase, estrogen maintains the thickened
endometrium, and progesterone causes it to develop blood vessels and secretory
glands (secretory phase). As the corpus luteum “starved” endometrium
degenerates and sloughs off, causing menstruation, the ischemic/menstrual
phase.
uterine prolapse- the descent of the cervix or entire uterus into the vaginal canal
due to weakened pelvic fascia and musculature and poor support from the
vaginal muscles and fascia.
polycystic ovarian syndrome- most common cause of anovulation and ovulatory
dysfunction in women. Defined as having 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. PCOS is associated with
metabolic dysfunction, including dyslipidemia, insulin resistance, and obesity.
One of the most common endocrine disturbances affecting women, especially
young women, and is a leading cause of infertility in the U.S. Strong genetic
component to PCOS, various features of the syndrome may be inherited. PCOS
patients are three times as likely to have insulin resistance, higher for obese
women. Tend to have increased leptin levels. Symptoms within 2 years of puberty
& include: dysfunctional bleeding or amenorrhea, hirsutism, acne, acanthosis
nigricans, and infertility. 60% are obese. Increased risk for gestational DM,
pregnancy-induced HTN, preterm birth, and perinatal mortality.
testicular cancer and conditions that increase risk- most common cancer in men,
age 15-35. Slightly more common on the right than on the left. 90% of testicular
cancers are germ cell tumors arising from the male gametes. Two types:
Seminomas-most common, least aggressive, make up 30-35% of testicular
cancers & Nonseminomas-include embryonal carcinomas, teratomas, and
choriocarcinomas, which are the most aggressive, but rare form of testicular
cancer. Risk factors include: genetic predisposition, history of cryptorchidism,
abnormal testicular development, HIV, AIDS, Klinefelter syndrome, and history of
testicular cancer. Can arise from specialized cells of the gonadal stroma-these
tumors, which are named for their cellular origins, are Leydig cell, Sertoli cell,
granulosa cell, and theca cell tumors and constitute less than 10% of all testicular
cancers.
symptoms that require evaluation for breast cancer- painless lump, palpable
nodes in the axilla, retraction of tissue (dimpling), chest pain, dilated blood
,vessels, edema, edema of the arm, hemorrhage, local pain, nipple/areolar eczema,
nipple discharge in non-lacting woman, pitting of the skin (like surface of an
orange peel), reddened skin, local tenderness and warmth, skin retraction,
ulceration.
signs of premenstrual dysphoric disorder- One of these symptoms must be
present for a diagnosis: marked affective lability, marked irritability or anger or
increased interpersonal conflicts, marked anxiety, tension. One of these must
also be present: decreased interest, difficulty concentrating, easy fatigability, low
energy, increase or decrease in sleep, feelings of being overwhelmed, physical
symptoms, such as: breast tenderness, muscle or joint aches, bloating or weight
gain. (Greater than 5 of these symptoms occur during the week before menses
onset, improve within a few days after menses onset, and diminish in the week
postmenses).
dysfunctional uterine bleeding- bleeding that is abnormal in duration, volume,
frequency, or regularity; and has been present for the majority of the previous 6
months. May be acute or chronic. PALM-COEIN System for classification of
abnormal uterine bleeding: PALM-structural causes: Polyp, Adenomyosis,
Leiomyoma, Malignancy. COEIN-nonstructural causes: coagulopathy, ovulatory
dysfunction, endometrial, iatrogenic, not yet classified. Increased endometrial
bleeding is correlated with a change from ovulatory to anovulatory cycles due to
high estrogen levels.
pathophysiology of prostate cancer- More than 95% of prostatic neoplasms are
histologically similar to adenocarcinomas and rely on androgen-dependent
signaling for their development and progression. Most of these neoplasms occur
in the periphery of the prostate. Prostatic adenocarcinoma is a heterogeneous
group of tumors with a diverse spectrum of molecular and pathologic
characteristics, and therefore clinical behaviors and challenges. The biologic
aggressiveness of the neoplasm appears to be related to the degree of
differentiation rather than the size of the tumor. Testicular testosterone provides
the main source of androgens in the prostate and is the major circulating
androgen, whereas DHT predominates in prostate tissue and binds to the
androgen receptors with greater affinity than does testosterone. Androgen
production outside of the testes, or extra testicular sources. Testosterone is
converted to dihydrotestosterone, DHT is the most potent intraprostatic
androgen.
HPV and the development of cervical cancer- almost exclusively caused by
cervical human papillomavirus (HPV) infection. HPV strains 16 & 18 are most
often implicated as causing 70% of all cervical cancers and also contribute to
many vaginal, vulvar, penile, anal, and oropharyngeal cancers. Most HPV
infections are cleared from the immune system; vast majority of infections do not
cause cervical cancer. Screening before age 21 not recommended. Women with
multiple sex partners are more likely to be exposed to high-risk HPV, but women
with only one lifetime sexual partner can also become infected. Transformation
zone is where the two cell types of squamous epithelium cells and columnar
, epithelial cells come together and this is where carcinoma in situ is most likely to
develop. PAP test or HPV screening necessary for early detection; 90% can be
detected by these. Viral DNA becomes integrated into the genomic DNA of the
infected basal cell of the cervix and directs the persistent production of viral
oncogenes. Persistence of infection with high-risk HPV is a prerequisite for the
development of cervical intraepithelial neoplasia, lesions, and invasive cervical
cancers.
Endocrine:
body’s process for adapting to high hormone levels- Feedback systems. Most
hormone levels are regulated by negative feedback, in which tropic hormone
secretion raises the level of a specific hormone. The elevated level of the specific
hormone then causes negative feedback, decreasing secretion of the tropic
hormone. Positive feedback systems, in which elevated hormone levels increase
a response which then further increases hormone secretion, is seen most often in
reproductive hormones. Negative feedback is the most common & occurs when a
chemical, neural, or endocrine response decreases the subsequent synthesis and
secretion of a hormone. Positive feedback occurs when a neural, chemical, or
endocrine response increases the synthesis and secretion of a hormone. Positive
feedback also occurs when an increased hormone level further increases the
synthesis and secretion of that same hormone. The sensitivity or affinity of the
target cell to a particular hormone is related to the concentration of receptors per
cell: the more receptors, the higher the affinity or the more sensitive the cell is to
the stimulating effects of the hormone. Thus the cell can adjust its sensitivity to
the concentration of the signaling hormone. hormone is distributed throughout
the body, only target cells with specific receptors for that hormone are affected.
Target cell response depends on blood levels of the hormone, the concentration
of target cell receptors, and affinity of the receptor for the hormone. Hormone
receptors of the target cell have two main functions: (1) to recognize and bind
with high affinity to their particular hormones and (2) to initiate a signal to
appropriate intracellular effectors. See Chapter 1 for cell signaling pathways,
particularly.
Cushing’s Syndrome- the clinical manifestations resulting from chronic exposure
to excess endogenous cortisol and is more common in women. Cushing’s
disease is excess endogenous secretion of ACTH. ACTH dependent
hypercortisolism (about 80%) results from overproduction of pituitary ACTH by a
pituitary adenoma (most common and can occur at any age) or by an ectopic
secreting nonpituitary tumor, such as a small cell carcinoma of the lung (more
common in older adults). ACTH-independent hypercortisolism (about 20%) is
caused by cortisol secretion from a rare benign or malignant tumor of one or both
adrenal glands (more common in children). A Cushing-like syndrome may
develop as a side effect of long-term pharmacologic administration of
glucocorticoids. With ACTH-dependent hypercortisolism, the excess ACTH
stimulates excess production of cortisol and there is loss of feedback control of
ACTH secretion. Whatever the cause, two observations consistently apply to
individuals with Cushing’s syndrome: 1.) They don’t have diurnal or circadian
