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Altered Reproductive Function.docx

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NURS 2090
Heather Helpard

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Altered Reproductive Function 1. Female Reproductive Function: External Genitalia: Mons pubis, labia majora/minora, vestibule, skene glands/bartholin glands for lube. 2. Female Reproductive Function: Internal Structures Uterus: 1.Inner endometrium: sloughed during menses. 2. muscular myometrium 3. outer perimetrium Ovaries: Estro/Progesterone/Andro 1. Stoma: supporting tissue 2. Interstitial cells: secrets estrogen 3. Follicles: ova/germ cells 4. Corpus Luteum: forms after the ovum has been released from ovarian follicle Pregnancy: hCG from zygote which acts on CL to maintain progesterone/estro Prolactin/ Oxytocin Estrogens Progesterone FSH LH Organ development, fat Secreted during Production of follicles LH surge releases the distribution, breast ovulation- menses from follicle development CL Ovulation, etc Thickens endometrium Oxytocin Prolactin Cervical mucous Maintains pregnancy by Posterior Pituitary, Anterior Pituitary, to alterations relaxing smooth contractions and milk allow lactation to muscles ejection (let down during occur lactation) Skin maintenance, bone Elevates core temp Resorption Retention of Na +H2O Produces NV, constipation, indigestion during pregnancy Ovulation 1. Follicular phase:  About 10 primary inactive follicles are stimulated by FSH/LH and become active secondary follicles.  Secondary enlarge and secrete estrogen/progesterone.  One becomes dominant and the rest atrophy (atretic)  Dominant continues to secrete estrogen which alerts pituitary to stop FSH production (↓FSH)  LH levels remain elevated and reach a LH surge (at the peak of estrogen secretion from the dominant follicle)  This LH surge allows the follicle to be released (ovulation) 2. Luteal phase:  Ruptured follicle forms a Corupus Luteum (CL), which secretes estrogen/progesterone  If pregnancy: progesterone from CLsupports pregnancy until placenta developed  If no pregnancy the progesterone/estrogen decrease and menses begins Endometrial Growth 1. Proliferative phase:  End of menstruation- ovulation  Estrogen supports the proliferation of the superficial layer of the endometrium  Its thin after menstruation then grows 6-8 X 2. Secretory phase:  Ovulation- beginning of menses  Progesterone/estrogen proliferate endometrium  Lining becomes thick and vascular  Ovum can now embed 3. Menstrual phase:  Absence of fertilization CLis useless. Disintegrates  Therefore decline in estrogen/progesterone  Shedding and menstruation. ** If the woman has issues with infertility it could have something to do with FSH/LH levels (especially with someone older, as the menses has slowed and the body wants to force it to continue, which creates higher than normal of both hormones). ** Temperatures rise during the LH surge and ovulation kits are what evaluate this hormone, as you will have about 24 hours to get pregnant. The increase in temp is only about 1 degree Male Reproductive Function 1. Testes- produce sperm 2. Epididymis- store/mature sperm 3. Vas Deferens 4. Seminal vesicles 5. Prostate 6. Penis **takes about 2 weeks to get a new batch of sperm Male Sex Hormones and Spermatogenesis 1. GnRH - stimulates FSH/LH release 2. FSH- acts on sertoli cells (in seminiferous tubules to secrete inhibin, which suppresses secretion of gonadotrophins) *role in spermatogenesis 3. LH- acts on leydig cells to secrete testosterone 4. Testosterone: a. Development of male organs, sperm, hair, deepens voice b. Protein metabolism c. Muscle mass production d. Skin thickness promotion e. Sebaceous gland activity 5. Inhibin- shuts off feedback to reduce LH release **Sadly men don’t have hormonal manipulations. Just evaluate sperm counts and select motile sperm to do artificial insemination ** Although low FSH/LH is linked to infertility also. Altered Reproductive Function Pathophysiology: 1. Hormonal imbalance: absence/irregular ovulation OR testosterone decreases which affect sperm production. 2. Motility impairment: Adhesions/obstruction of cervix to ovary which blocks passage way for oocyte/sperm. Includes inhospitable cervical mucus.(IVF takes away this issue) 3. Immune problems: Antibodies formed which attack male sperm. General Manifestations: 1. Infertility 2. exercise. They can give CNS alterations of pregnancy, stress or extensive 3. Pain: dysmenorrheal (during menses), dysparenia (during sex) Diagnostic Criteria:  History and physical examination  Determination of ovulation (looking for basal body temp)  Sperm analysis  Laboratory hormone levels, antibodies  Imaging studies (looking for disease/ adhesions)  Laparoscopy- incision in the abdomen, views peritoneal cavity/ abdominat structures outside the uterus/fallopian tubes  Hysterosalpingography- injecting radiopaque material into uterus/fallopian tubes to see obstructions.  Genetic testing Treatment:  Dependent upon cause  Infection  Hormone imbalance  Motility problems  Immune problems  Supportive counseling and education  Reproductive technologies Pelvic Inflammatory Disease Pathophysiology:  The result of a sexually transmitted infection of the reproductive tract (can go as far as the peritoneal cavity)  Inflammation and immune response  Fallopian tubes obstructed with purulent exudates  Scar formation (especially if it travels to the fallopian tube b/c it blocks egg/sperm) Clinical Manifestations:  Asymptomatic in early stages  Pelvic and lower abdominal pain (extreme)  Purulent cervical discharge  Cervical tenderness (cervitis)  Fever  Malaise  Painful intercourse  Tachycardia (due to inflammation and edema)  Potential complications of PID: ectopic pregnancy, absesses, adhesions, infertility Diagnostic Criteria:  History  Physical examination/laparoscopy  Lower abdominal tenderness  Adnexal tenderness (ovaries)  Cervical motion tenderness  Laboratory studies  ESR or CRP (elevated)  STD screening (especially, gonorrhea, Chlamydia) Treatment  Treat infected patient and partners (antibiotics)  Hospitalize, if high risk  Ultrasounds  No sex for period of healing (6 months!) Polycystic Ovarian Syndrome Pathophysiology:  Acondition of excess androgen production from the ovaries  Exact cause unknown; genetic?  Anovulation (absence of ovulation) due to lack of follicular maturation produces bilaterally distended and cystic ovaries  Relationship between high androgen levels and insulin resistance (lead to diabetes)  Note: Pituitary gland secretes high LH levels, and ovaries make androgens. Presence of FSH allows development of follicles but no maturation. Absense of ovulation makes estrogen alter GnRH to release more LH. FSH gets suppressed. Clinical Manifestations:  Menstrual irregularities (prolonged and irregular)  Hirsutism: excess facial and body hair  Acne  Male-pattern baldness  Obesity  Acanthosis nigricans (darkened, velvety skin at nape of neck, armpits, inner thighs, vulva, under br
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