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Conj 403 > Final - Amanda > Flashcards

Final - Amanda Flashcards

1
Q

Steroid Hormones

A
  1. Hormones are non-polar and can diffuse through membranes. 2. Regulation is through synthesis. Signal by binding to intracellular or “nuclear receptors”. 3. Often are modified by enzymes at target cells. Example: Testosterone is converted by 5-alpha reductase to the more potent form DHT (dihydrotestosterone). Androgens converted to estrogen through enzyme aromatase.
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2
Q

Types of steroid hormones

A
  1. androgens: androstenedione, DHEA, testosterone, DHT. 2. Estrogens: estrone, estriol, estradiol 3. progestogens: progesterone
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3
Q

Estrogen is inhibiting gonadotropin secretion (negative feedback effect).

A

B and E. During dominant follicle maturation of follicular phase and during the luteal phase

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4
Q

Estrogen stimulates gonadotropin secretion (positive feedback effect).

A

C. LH surge and ovulation phase.

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5
Q

This time corresponds to dominant follicle selection.

A

B. During growth phase days 7-14

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6
Q

This time corresponds to the first day of menstruation.

A

A. Menstrual phase.

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7
Q

Granulosa cells proliferate in response to FSH only, not LH.

A

B and also A.

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8
Q

Granulosa cells respond to both FSH and LH.

A

C

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9
Q

Negative feedback by bothestrogen and progesterone prevents ovulation.

A

E. secretory phase of uterine cycle and luteal phase of hormonal.

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10
Q

Corpus luteum is degenerating

A

F

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11
Q

Gonadotropin levels rise due to release from negative feedback inhibition.

A

A and F. In uterine cycle is menstual phase. and is Follicular phase in hormonal.

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12
Q

Progesterone promotes secretion by endometrial glands

A

E. secretory phase of uterine cycle

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13
Q

Estrogen promotes proliferation in the endometrium

A

B and C. proliferative stage of uterine cycle.

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14
Q

This time corresponds to rupture of the dominant follicle.

A

D. LH surge and ovulation day 14.

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15
Q

Disfunction in meiosis

A

nondisjunction is when chromosome doesn’t separate at one of the divisions and leads to the disorder aneuploidy. Can occur at first or second division. Trisomy 21 causes Down Syndrome (3 chromosome 21). Older women carry greater risk for aneuploidy.

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16
Q

Karotyping Fetus

A

Karotype looks at all chromosomes in cells.

Karyotyping requires fetal cells be obtained by amniocentesis or chorionic villus sampling, and both methods are invasive and carry a risk for miscarriage or infection.

New method that is non-invasive is cell-free fetal DNA analysis, can be done earlier than the others and only involves a blood draw.

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17
Q

Hormone regulation : pulsitile secretion of GhnR

A

Gonadotropins are FSH and LH. travel in general circulation to stimulate gonadal hormone production.

Remember that steroid and gonadotropins have negative feedback effects.

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18
Q

Hormone regulation: continuous GnRH

A

pulsatile GnRH stimulates gonadotropins.

However, continuous GnRH inhibits gonadotropins. Leuprolide is a GnRH agonist which causes continuous GnRH and is used to turn off reproductive function. Used in precocious puberty, androgen depravation therapy (prostate cancer), cycle control (IVF).

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19
Q

GNrH secretion during all stages of life

A

GnRH is master regulator. High secretion occurs before birth during sexual differentiation. GnRH is low during childhood and high again after puberty.

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20
Q

leptin

A

Since 1800’s mean age of menarche has dropped. Relates to nutrition. Leptin is a part of a negative feedback loop to control adiposity. Obese mutant mouse fails to make leptin and suffers from hypogonadotropic hypogonadism. Low levels of gonadotropins due to lack of GnRH levels. Leptin is permissive for GnRH secretion occurring at puberty. In absolute leptin deficiency (obese mouse) have infertility. Back in the 1800’s nutrition was poor and leptin secretion was low so puberty occurred much later.
Human examples of hypoleptinemia in women. Very very low body fat level with low leptin secretion and they experience amenorrhea.

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21
Q

Route of sperm

A

Sperm develop in testes in seminiferous tubules. Move to epididymis to ductus deferens (2), to ejaculatory duct (2- contains sperm and secretion of seminal vesicle) then finally to the urethra. Movement of sperm along the vas deferens depends upon smooth muscle contraction.

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22
Q

Semen composition

A

Male semen is spermatozoa and seminal fluid. Seminal fluid is from bulbourethral glands, prostrate glands and seminal vesicles (2 of them).

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23
Q

Benign Prostatic Hypertrophy

A

is the enlargement of the prostate gland with age (BPH).

Causes urinary symptoms such as difficulty in urination and painful urination.

Treated with alpha-adrenergic antagonists, Tamsulosin through relaxation of smooth muscle in urethra. Also have 5-alpha reductase inhibitors, finasteride, that prevent conversion of testosterone to dihydrotestosterone.

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24
Q

Prostate cancer

A

tends to be slow growing. Effect of increased PSA testing has not affected mortality of prostate cancer. In many cases the best treatment is to just leave the prostate alone.

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25
Q

Spermatogenesis

A

spermatogonia (diploid) cells undergo mitosis. Differentiation into primary spermatocyte. Meiosis I and II to spermatids and differentiation into spermatozoa. Development of spermatid to spermatozoon involves formation of flagella. Acrosome in head of sperm contains digestive enzymes and is important in fertilization.

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26
Q

Leydig cells

A

make testosterone. Located outside seminiferous tubule

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27
Q

Sertoli cells

A

Located in seminiferous tubule. Wrap around developing germ cells.

Functions: create blood-testis barrier with tight junctions, nourishing paracrine signaling required for spermatogenesis, have receptors for FSH and testosterone (necessary for spermatogenesis), produce binding protein (androgen-binding protein), and produce hormones (inhibin involved in negative feedback and mullerian inhibiting substance).

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28
Q

Tight junctions in semineferous tubules

A

create basal and central compartment. Central compartment has meiosis and contains spermatocytes, spermatids and spermatozoon. Basal compartment undergoing mitosis and contains spermatogonium.

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29
Q

Male hormonal regulation

A

Leydig cells: binds and responds to LH to produce testosterone. Testosterone stimulates sertoli cells.

sertoli cells: binds to and responds to FSH to stimulate spermatogenesis and inhibin (negative feedback to anterior pituitary).

Negative feedback inhibition.

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30
Q

Erection

A

vascular function. smooth muscle relaxation. Fill with blood and become engorged through relaxation of smooth muscle. Maintenance of erection is through compression of veins.
Corpus cavernosa: two. vascular spaces.
Corpus spungium: behind and form gland at bottom

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31
Q

Autonomic control of erection

A

NANC (nonadrenergic, noncholinergic) neurons: release nitric oxide as neurotransmitter. Smooth muscle relaxation (through cGMP) to dilate arteries (through lower of Ca++) and causes erect penis.

sympathetic neurons: release norepinephrine as neurotransmitter. Smooth muscle contraction constricts arteries and penis is flaccid.

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32
Q

Erectile disfunction

A

problems with attaining or sustaining an erection. Oral drugs are phosphodiesterase inhibitors. Phosphodiesterase cleaves cGMP which normally causes smooth muscle relaxation and erection. Works through the NANC pathway.

PDE inhibitors include sildenafil, vardenafil, tadalafil, avanafil. Don’t cause an erection, just potentiate the affects of arousal.

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33
Q

Ejaculation

A

release of semen.

Semen first moves into urethra which involves contraction of smooth muscle around ducts (vas deferens, ejaculatory duct, glands and internal urethral sphincter which prevents semen from entering bladder) and depends on sympathetic input.

Release of semen from penis involves sympathetic efferents stimulating contraction of smooth muscle in the urethra and contraction of skeletal muscle in pelvic floor.

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34
Q

Sexually indiferent stage

A

(week 6)

Period of time where the embryo either develops male or female structures.

Wolffian (mesonephric) ducts give rise to male gonad structures and are more medial, and Mullerian (paramesonpehric) ducts gives rise to female gonad structures and are more lateral.

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35
Q

Sexual determination for males

A

depends on presence of Y chromosome. The Y chromosome has a sex-determining region called SRY which initiates testis development. The absence of the SRY region directs the gonads to develop as ovaries.

Leydig cells make testosterone which promotes Wolffian duct development. The Wolffian duct then differentiates to form the epididymis, vas deferens, seminal vesicle, and ejaculatory duct.

Sertoli cells make MIS (Mullerian Inhibiting Substance) which causes the Mullerian ducts to regress/degenerate.

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36
Q

Sexual determination for females

A

absence of SRY gene: gonad develops as an ovary

Lack of Sertoli cells promotes no MIS so Mullerian duct develops and gives rise to fallopian tubes, uterus, and the upper part of the vagina.

Lack of Leydig cells causes no testosterone production and Wolffian ducts degenerate.

37
Q

Disorders of sexual development

A

androgen insensitivity syndrome and 5-alpha-reductase defeciency

38
Q

Androgen insensitivity syndrome

A

Complete AIS has no activity in receptor, develops as a women but has amenorrhea (lack of menstruation). Usually have sparse pubic and axillary hair because the growth of hair depends on androgen signaling.

Gonad is testes which are in abdomen, Sertoli cells degenerate Mullerian ducts and Leydig cells make testosterone which doesn’t work so Wolffian ducts degenerate. Uterine development is prevented by MIS hormone released from Sertoli cells.

Testosterone from testes is converted to estrogen through aromatase which is responsible for female secondary sexual characteristics.

39
Q

Cryptorchidism

A

the failure of testes to descend to scrotum and is associated with development of testicular cancer.

Occurs in complete AIS and normally just remove testes in young adulthood (after puberty). Then maintained on estrogen replacement therapy.

40
Q

5-alpha reductase defeciency

A

5-alpha reductase: Causes conversion of testosterone to DHT which is responsible for development of penis and prostate gland.

With deficient reductase activity, result is hypospadias (urethra on underside of penis) and female external genitalia at birth.

mullerian ducts degenerate and Wolffian ducts development

At puberty have male development because of increased testosterone.

DHT causes prostrate growth. In BPH use drugs that limit production of DHT, 5-alpha-reductase inhibitors

41
Q

male vs female physiology

A
  1. spermatogonia proliferate at puberty and continue through life. Oogonia proliferates before birth and stop before birth. In follicle have primary oocyte in meiotic unrest.
  2. In males 1 spermatocyte gives 4 spermatozoa. In females one oocyte develops one ovum. Other polar bodies are non-functional and just contain chromosomes.
  3. Males produce millions of spermatozoa and females only produce a few quality ovum.
42
Q

Follicle development/initial development

A

Can occur independent of hormones and at any time during the monthly cycle.

Primordial follicle: quiescent non-developing. Oocyte in meiotic arrest with follicle cells.

Growing follicle: Develops from primordial follicle in response to local signals that are not well-defined. Follicle cells differentiate to granulosa cells. oocyte enlarges and develops zona pellucida.

Antral follicle: presence of antrum and theca cells.

43
Q

Atresia

A

follicle degenerates because of lack of hormonal support.

44
Q

Number of ovulations in lifetime

A

Only have 300 or so ovulations in lifetime. Fewer ovulations are associated with lower risk of ovarian cancer.

45
Q

Follicular Phase or Growth Phase

A

Day 1-7: Increases in FSH and LH due to release of negative feedback inhibition. At day 7 a dominant follicle is selected. LH cells stimulate thecal cells to produce androgen precursor. FSH stimulates granulosa cells and expresses aromatase which converts androgen to estrogen. Slight increase in estrogen levels.

Days 7-14: Negative feedback due to increasing estrogen levels, limits gonadotropin secretion while the dominant follicle enlarges to become a mature follicle. Granulosa cells secrete inhibin which inhibits FSH secretion

46
Q

LH surge and ovulation

A

Occurs at day 14 when the follicle ruptures and releases the egg to the fluid surrounding the ovary. Positive feedback due to high estrogen levels (must reach a certain threshold to switch to positive feedback) increases secretion of hormones, including LH. LH in turn stimulates more estrogen production and a small increase in progesterone secretion.

47
Q

Luteal phase

A

Day 14-28. Remaining cells of the follicle differentiate into the corpus luteum which secretes progesterone and estrogen causing negative feedback inhibition of LH and FSH. If a fertilized embryo implants in the uterus, the hormone chorionic gonadotropin is made, which stimulates growth of the corpus luteum. If implantation doesn’t occur, a drop in LH below a certain levels causes the corpus luteum to regress releasing the negative feedback inhibition and allowing FSH and LH to steadily increase, starting a new cycle.

48
Q

Uterine cycle: proliferative phase

A

high estrogen levels stimulate endometrial proliferation in the functional layer. induction of progesterone receptors, thin, watery cervical mucus. Fertilization

49
Q

Uterine cycle: secretory phase

A

high progesterone prevents proliferation and causes secretion of nutritive substances by endometrial glands.

50
Q

Uterine cycle: menstraul phase

A

drop in estrogen and progesterone trigger menstruation, which is the shedding of the functional layer of the endometrium. Early part have vasoconstriction and ischemia. Late phase have vasodilation and bleeding and myometrial contractions

51
Q

menorrhagia

A

excessive menstrual bleeding

52
Q

Leiomyoma

A

“fibroids” or benign growth(s) in myometrium, where it generally stays confined to. Can cause menorrhagia when endometrium abnormally grows over the fibroids. More common in older women so usually treatment is a hysterectomy (removal of uterus).

53
Q

Unopposed estrogen

A

More common in younger women and occurs in polycystic ovary syndrome (PCOS). Disorder of anovulation and there is no transition to the luteal or secretory phase. Therefore, have an ongoing situation resembling the later part of the follicular phase when estrogen levels are high but progesterone is low. Ongoing proliferation due to high estrogen that isn’t stopped by progesterone. High levels of proliferation increases risk for endometrial cancer. Treatment is hormonal contraceptives that contain progesterone which mimics the luteal phase and limits proliferation in the endometrium.

54
Q

anovulation

A

lack of ovulation

55
Q

prolactin effects

A

involved in lactation, stimulates breast growth (during pregnancy), stimulates milk synthesis (during lactation) and inhibits GnRH secretion.

56
Q

Stimulation of milk production

A

Two effects.

First, suckling stimulates nipple mechanoreceptors which stimulate magno-cells to release oxytocin from the posterior pituitary. Oxytocin causes milk ejection in which myoepithelial cells contract to push milk from the glands into the breast ducts.

The second mechanism involves parvocells which releases dopamine at the median eminence and now acts as a hormone to travel to the anterior pituitary via the hypophyseal portal vessel. There dopamine inhibits prolactin secretion. Suckling inhibits dopamine secretion, increasing prolactin secretion to stimulate milk production in the breast.

57
Q

Hyperprolactinemia

A

Prolactin inhibits GnRH secretion to cause amenorrhea, anovulation, and occasionally galactorrhea (abnormal milk production).

Low GnRH leads to low gonadotropin secretion (LH, FSH) which causes low gonadal steroid production and infertility is due to hypogonadotropic hypogonadism.

Most common cause is prolactinoma which is a benign tumor that is contained to anterior pituitary, causing prolactin secretion. Drug-induced hyperprolactinemia is caused by dopamine antagonist drugs.

Treatment is to use dopamine agonist to limit prolactin secretion, including bromocriptine and cabergoline (high doses for Parkinson’s and low doses for prolactinoma).

58
Q

PCOS diagnosis

A

Diagnosis involves two of the following signs/symptoms.

Chronic anovulation (experienced as amenorrhea or oligomenorrhea which is irregular menstruation), hyperandrogenism (excess secretion of androgen hormones that results in abnormal hair growth typical in a man and is called hirsutism and also an increase in acne), polycystic ovaries (enlarged, multiple immature follicles, hyperplasia of theca cells, fewer granulosa cells).

Associated signs/symptoms are insulin resistance (usually only in overweight women with metabolic disorders) and hyperinsulinemia (higher than normal insulin secretion).

59
Q

Endocrine disfunctions in PCOS

A

Excess of LH causes theca cell proliferation and secretion of androgens.

Insufficient FSH doesn’t stimulate granulosa cells which express aromatase, the enzyme necessary for the ovary to produce estrogen.

Peripheral conversion of androgens to estrogen in adipose through peripheral aromatase can cause abnormal negative feedback loop.

Insulin resistance leads to hyperinsulinemia which further causes hyperandrogenism

60
Q

PCOS treatment for women who do not want to conceive

A

For women who do not want to conceive: weight loss, metformin and hormonal contraceptives. Estrogen and progesterone restore appropriate negative feedback inhibition and reduce LH secretion and androgen production. Also used to prevent uterine problems due to unopposed estrogen with PCOS which causes menorrhagia (excessive menstrual bleeding) and an increased risk of endometrial cancer. HC either block or cause regular menstruation to prevent excessive proliferation.

61
Q

PCOS treatment for women who do want to conceive

A
  1. weight loss
  2. clomiphene: first choice. SERM selective estrogen receptor modulator. Works as an estrogen antagonist in the hypothalamus and anterior pituitary to block the abnormal negative feedback of estrogen. Random side note: With longer half life you may have too much FSH resulting in multiple follicles maturing leading to multiple ovulation.
  3. Aromatase inhibitors (letrozole): Aromatase inhibitor decreases estrogen synthesis (conversion of androgen to estrogen) and inhibit abnormal negative feedback. Benefit of aromatase inhibitor is that it has a shorter half-life than clomiphene, which allows for normal estrogen action later in the cycle.
  4. Metformin: only used in certain overweight individuals and usually along with another option.
  5. Exogenous FSH: Menotropin was the first treatment developed and was a mixture of gonadotropins (LH and FSH) purified from the urine of menopausal women. Urofollitropin is FSH purified from urine. Follitropin is most recent and is purified recombinant FSH. Risk for multiple ovulation and multiple pregnancy and for ovarian hyperstimulation syndrome (OHSS) which can cause edema, nausea, abdominal pain, clotting abnormalities, respiratory distress and renal failure. Monitor estrogen levels.
  6. surgery: damage ovary which stops androgen production releasing anterior pituitary from negative feedback.
62
Q

HC MOA

A

negative feedback inhibition of gonadotropin secretion to block the luteal phase then LH surge and suppress ovulation.

Alternatively, uterine effects influence how sperm move. Sperm are deposited in the vagina and must traverse the cervix. In the follicular phase, estrogen promotes the production of thin watery mucus by the cervical glands. In contrast, progesterone causes thick cervical mucus which decreases ability of sperm to traverse surface.

Finally, HC reduce endometrial growth so it is theoretically possible that they may clock conception by interfering with implantation, but it is difficult to know what role if any this mechanism plays.

63
Q

combination HC

A

estrogen and progestin (drug that binds to progesterone receptors) delivered in pills, patch (lipophilic so can be delivered topically), or vaginal ring. Mid-cycle bleeding and withdrawal bleed (during placebo pills). Continuous use are designed for women who suffer from menorrhagia (excessive menstrual bleeding) or dysmenorrhea (painful menstruation).

64
Q

progesterone only HC

A

low dose/mini-pills (useful in lactating women because high levels of estrogen or progesterone inhibits milk synthesis) or long acting including Depo-provera (injection), implantable rods, progesterone-releasing IUD. LARC long-acting reversible contraceptive advantages include excellent effectiveness and usually cause a lack of menstration (inhibits endometrial proliferation). Concern with LARC is the lack or estrogen production can cause a decrease in bone density.

65
Q

Benefits HC

A 
effective contraception (LARC are most effective). 
Non-contraceptive benefits include treatment of PCOS, decreased acne, reduction of endometrial proliferation (menstrual dysfunction, reduces menorrhagia and dysmenorrhea as well), decreased risk of endometrial and ovarian cancer.
66
Q

Risks with HC

A

cardiovascular risks: promote thrombosis consequences being venous thromboembolism (VTE clot in venous system), pulmonary embolism, myocardial infarction or stroke. Pregnancy increases risk of cardiovascular events to a greater extent but overall risks are so low. Absolute risk is very low.

Breast cancer: estrogen and progesterone promote breast growth. No increase in risk of breast cancer among current and former users (studies focused on older women). Absolute risk very low.

67
Q

Timeline for emergency contraceptive

A

Timeline: sperm is viable in female reproductive tract for 5 days. Egg is only viable for 24 hours after ovulation. Theory is that you can prevent fertilization by blocking or delaying ovulation.

68
Q

Plan-B

A

levonorgestrol (high dose progestin). Only works if taken before LH surge and works by negative feedback inhibition to inhibit LH secretion and block LH surge.

69
Q

Ella

A

ulipristal acetate. “selective progesterone receptor modulator”. Blocks the small increase in progesterone right before ovulation, which is necessary for ovulation to occur. Can be taken after the beginning of the LH surge but is only effective when taken before the peak of the LH surge.

70
Q

Mifepristone

A

Progesterone antagonist used in medical abortion to terminate pregnancy in first seven weeks.

At early stage progesterone is acting to maintain endometrium to support a pregnancy. Also prevents myometrium from contracting.

Standard procedure: administer mifepristone which is followed by prostaglandins which induces myometrial contractions. Mifepristone induces the shedding of the endometrium.

71
Q

Events of fertilization

A

occurs at end of fallopian tube near the ovary.
1. Sperm: When they reach the egg they bind to the zona pellucida and causes the acrosome reaction (ruptures). Acrosome is a large vesicle in head of sperm that contains digestive enzymes. Release of digestive enzymes enables the sperm to penetrate zona pellucida.

  1. Fertilization occurs when sperm membrane fuses with the egg membrane. This triggers a reaction in the ovum causing exocytosis of vesicles to modify zona pellucida.
  2. Zona hardening: result is that any other sperm bound will fall off and others are blocked from fusing.
  3. Sperm egg fusion stimulates meiosis II. Both nuclei fuse to give zygote which can divide.
  4. Egg activation occurs
72
Q

Implantation

A

Implantation occurs 6-7 days after fertilization. Zona pellucida is helping to prevent implantation early.

Cleavage: First cell divisions that are occurring in conceptus without any growth.

73
Q

Implantation: blastocyte

A

Two types of cells. Outer layer is called trophoblast and forms extra-embryonic tissue (chorion). Small group of cells inside is called inner cell mass and forms embryo.

74
Q

Implantation: zona hatching and adherence

A

breaks out of zona pellucida. Is very sticky at this point and readily implants.

Adherence to the endometrium is through the trophoblast. This stimulates proliferation of the trophoblast cells into two parts.

Syncytial trophoblast is invasive and digests its way into the endometrium. Digestion of the endometrial tissue creates spaces known as lacunae. It produces chorionic gonadotropin which is an analogue of LH, meaning it binds to and stimulates the LH receptor. CG is necessary to stimulate and maintain the corpus luteum.

Cellular trophoblast proliferates and forms branched chorionic villi.

75
Q

Placenta

A

Organ of exchange between developing fetus and mother. Also a site of hormone synthesis.
Forms from the trophoblast and the endometrium (also known as the decidua).
Two parts: fetal (chorion) is made up of chorionic villi that protrude into lacunae and the decidua. The maternal part is formed from the decidua which is derived from endometrium and promoted by progesterone.
Development of amnion: forms around developing embryo and is fluid filled

76
Q

Hormonal changes during pregnancy

A

Estrogen and progesterone are steadily increasing. Source for first trimester is corpus luteum. After 8 weeks the placenta takes over production.

During gestation, progesterone promotes smooth muscle relaxation in the myometrium.

Chorionic gonadotropin (HCG) is an LH analogue made by trophoblast that stimulates corpus luteum. Used as an assay for pregnancy test

77
Q

Parturition

A

Delivery of infant and placenta.
Positive feedback loop. Coordinated by estrogen. Effects:

  1. myometrial proliferation
  2. stimulates formation of gap junctions that allow electrical coupling of cells in smooth muscle of myometrium.
  3. Stimulates increased oxytocin receptors expression in myometrium. Oxytocin causes contractions.
  4. Stimulates synthesis of enzymes involved in prostaglandin synthesis. Prostaglandins stimulate cervical ripening, which is the breakdown of cervical connective tissue allowing it to become soft and flexible. During labor prostaglandins stimulate myometrial contraction.
78
Q

Lactation

A

Both gonadal steroids stimulate breast growth. Progesterone stimulates growth of milk-producing cells and estrogen stimulates growth of duct cells and secretion of prolactin. In a non-lactating woman, most of the tissue in the breast is adipose tissue.

79
Q

Structure of the breast

A

Milk is produced by secretory structures known as alveoli. Alveoli are arranged in clusters called lobules. The lobules are connected to outlets at the nipple by ducts. The alveoli are surrounded by special contractile cells known as myoepithelial cells.

80
Q

Milk ejection reflex

A

When myoepithelial cells contract, milk is pushed out of the alveoli and into the ducts, where it can easily be sucked out by the infant.

81
Q

Congenital Adrenal hyperplasia

A

Problems with sexual differentiation of XX infants occur when excess androgens are produced during development. This can be due to an adrenal tumor in the mother, but occurs most often in the disorder known as congenital adrenal hyperplasia.

In this inherited condition, there are defects in the enzymatic pathways that produce cortisol. Because cortisol is secreted at a lower level than normal, it cannot exert negative feedback regulation on the secretion of the pituitary hormone ACTH, which stimulates hormone production by the adrenal gland. Instead of making cortisol, the adrenal glands produce large amounts of androgens, which have the effect of masculinizing XX females with this condition.

In XY males, this disorder leads to precocious sexual development.

82
Q

orchiopexy

A

Surgical correction of cryptorchidism done ideally before 2 years of age

83
Q

Germ cell tumorss

A

vast majority of cancers 95%. cancer arises from cells that will give rise to sperm. chemotherapy drug cisplatin has proved to be very effective in the treatment of testicular cancer.

84
Q

carcinoma in situ

A

another term for non-invasive breast cancer.

85
Q

Surgical treatment of breast cancer

A

either mastectomy (removal of the breast) or lumpectomy, in which the tumor and surrounding tissue are removed, but the breast is spared. Lumpectomy is usually followed by radiation therapy to eradicate any residual diseased cells. Larger tumors, more advanced tumors, or node-positive cancer (involving spread to adjacent lymph nodes) will require adjuvant therapy. Adjuvant therapy refers to any of the various systemic therapies: chemotherapy, hormone therapy, or trastuzumab.

86
Q

Breast cancer drug treatment

A

If a tumor is hormone-positive (over-expresses estrogen receptors), then it is appropriate to treat it with drugs that interfere with estrogen, such as tamoxifen (which is a selective estrogen receptor modulator; SERM) or letrozole (an aromatase inhibitor that prevents estrogen synthesis). Tumors that are positive for HER2 are treated with trastuzumab (tradename: Herceptin), an antibody-based drug that binds to the receptor and prevents cell growth.

87
Q

Pelvic inflammatory disease

A

acute infection of the upper reproductive tract in women, namely endometritis (infection of the endometrium), salpingitis (infection of the fallopian tubes), oophoritis (infection of the ovaries) and sometimes peritonitis.

88
Q

Endometriosis

A

disorder in which endometrial tissue is found in ectopic locations, usually in the pelvic cavity. Endometriosis can be treated surgically, or with drugs that decrease estrogen levels such as oral contraceptives or the GnRH agonist leuprolide.

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