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234 Cards in this Set
- Front
- Back
The menstrual cycle..bleeding and fertile times
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28 day cycle
Day 1-5 bleeding Day 11-15 fertile |
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For proper menstruation..need proper function of...(brief)
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proper function of
hypothalmus pituitary gland uterus |
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10 Steps: Menstrual Cycle Step 1
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1. The hypothalamus releases GnRH (Gonadotropin‐
Releasing Hormone). |
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Menstrual Cycle Step 2
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2. The pituitary secretes FSH and LH.
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Menstrual Cycle Step 3
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3. The FSH and LH stimulate follicle growth.
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Menstrual Cycle Step 4
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4. The follicles start to make estradiol. Several follicles
begin to grow with each cycle, but usually only one matures. |
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Menstrual Cycle Step 5
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5. Around day 12 estradiol levels rise steeply.
Rising estradiol stimulates a LH surge by positive feedback. |
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Menstrual Cycle Step 6
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6. The LH surge triggers ovulation: the follicle ruptures,
releasing the secondary oocyte. |
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Menstrual Cycle Step 7
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7. The follicle left in the ovary forms the corpus luteum,
which secretes progesterone and estradiol. |
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Menstrual Cycle Step 8
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8. Rising progesterone and estradiol levels stimulate
thickening of the uterine wall, or endometrium. |
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Menstrual cycle-Step 9
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9. If pregnancy occurs, the corpus luteum continues
secreting progesterone and estradiol to maintain the endometrium; otherwise it disintegrates and hormone levels drop, resulting in the loss of endometrial tissue as menstrual flow. |
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Menstrual cycle-step 10
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10. This continues for about 450 cycles, then women enter menopause.
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Dysfunction of menstrual cycle: what is painful period?
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dysmenorrhea
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Subcategories of dysmenorrhea: first one
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primary and secondary
primary: painful menstruation associated with the release of prostaglandins in ovulatory cycles, but not with pelvic disease, no other cause identified |
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Subcategories of dysmenorrhea: secondary
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Secondary: pelvic pathology
i.e. IUD, PID, endometriosis |
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What are some common causes of primary dysmenorrhea?
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-primarily the result of the effects of excessive endometrial prostaglandin production by uterus, enhanced by progesterone
-prostaglandin is a potent myometrial stimulant and vasoconstrictor -increased levels of vasopressin from uterus --> increased contraction -myometrial contraction: altered blood flow (constriction of arterioles) --> uterine ischemia --> pain |
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Amenorrhea: difference between two categories
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Amenorrhea: lack of menstruation, the most
-Primary: failure of menarche, period never started -Secondary: absence of menstruation for a time equivalent to three or more cycles or 6 months who have previously menstruated (more common), most common cause is pregnancy |
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Primary amenorrhea: 4 categories of causes
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1) hypothalamus
2) ovary 3) anterior pituitary 4) uterus/vagina ..primary amenorrhea usually r/t issues of structures or hormones |
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Primary amenorrhea: break down causes of hypothalamus
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Primary Amenorrhea: hypothalamus causes:
-No GnRH release |
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Primary amenorrhea: break down of causes from Ovary
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Primary Amenorrhea f/ ovary:
-no ovaries -no gametes -no follicle/follicular development -no estrogen release |
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Primary Amenorrhea: anterior pituitary causes
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-no FSH or LH release
..could be from congenital defect ..could be from tumor on pituitary ..damage to pituitary i.e. hydrocephalus ..if not released, no progression down pathway |
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Primary Amenorrhea: uterus/vagina causes
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-absent uterus and/or vagina
-infantile uterus |
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2 syndromes possibly r/t primary amenorrhea
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1) Turner's Syndrome: genetic d/o, may cause X chromosome without matching X
2) Androgen sensitivity syndrome: have XY (male), but body doesn't respond to testosterone so no male phenotype, externally female but no ovaries |
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Secondary amenorrhea: general list of causes
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Hypothalamus
Ovary Anterior Pituitary Uterus |
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Secondary amenorrhea: patho from high prolactin
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secondary amenorrhea:
-overproduction of prolactin by the pituitary -may lead to decreased GnRH by the hypothalamus -result is reduced FSH and LH by anterior pituitary -causing amenorrhea and annovulation |
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secondary amenorrhea: hypothalamus causes
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-decreased GnRH release
-structural change -elevated prolactin -elevated estrogen and progesterone (i.e. from pregnancy, the pill, stress, weight loss, excessive exercise) |
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Secondary amenorrhea: ovary causes
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-oversecretion of E/P (estrogen and progesterone), which inhibits GnRH
-undersecretion of E/P (not responding to GnRH) -premature ovarian failure -menopause -tumor -ovary removal |
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Secondary amenorrhea: ovary causes..relationship b/w E/P and GnRH
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-oversecretion of E/P --> inhibits GnRH
-undersecretion of E/P ---> doesn't respond to GnRH |
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Secondary amenorrhea: anterior pituitary causes
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-decreased FSH/LH
-structural cause |
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Secondary amenorrhea: uterus causes
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-hysterectomy
-endometrial ablation or adhesions |
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Most common causes of seondary amenorrhea
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-pregnancy
-hypothyroidism (assoc w/ high prolactin) -hyperprolactinemia -HPO interruption secondary to excessive exercise, stress, weight loss, and PCOS |
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Abnormal Uterine bleeding-how is it dx?
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dx of exclusion: look for fibroids, polyps, clotting, infection, pregnancy, ovarian cysts, bleeding d/o
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abnormal uterine bleeding-what is it?
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heavy or irregular bleeding in the absence of organic disease, such as submucous fibroids, endometrial polyps, blood dyscrasias, pregnancy, infx, or systemic disease
|
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Is abnormal uterine bleeding common?
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Yes, affects 15-20% of women at some time in menstrual life, accounts for 70% of hysterectomies, near all endometrial ablation procedures
-perimenopausal women most affected |
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What are some chronic conditions that can cause or are assoc w/ abnml uterine bleeding?
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-chronic conditions
-adrenal conditions -thyroid d/o -liver disease -DM -obesity -HTN |
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What is a common cause of abnormal uterine bleeding in perimenopausal women? patho
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Hormonal imbalance
-imbalance of estrogen/progsterone -decrease in progesterone -estrogen releases normally, uterus builds up without sufficient progesterone counter --> longer cycles and heavier periods due to uterus wall f/ estrogen |
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abnormal uterine bleeding in postmenopausal women?
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postmenopausal women 1 year after cessation of periods-worry about malignancy, concern
|
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What is a normal vaginal pH?
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3.8 - 4.8
|
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What condition is often caused by disruption in vag pH? Implications for too high? Too low?
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pH is often changed in vaginitis
-normal 3.8-4.8 -increase in pH: environment for bacteria, vaginosis seen with 5.0-6.0, trichimonus -decrease in pH (under 4.5) prone to yeast |
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What are the 4 female -itis talked about in class?
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Bartholinitis
Vulvo-vestibiulitis Vaginitis Cervicitis |
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How is pH of vag regulated? What is its purpose
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the pH of the vagina depends on cervical secretions and the presence of normal flora that help maintain an acidic environment
-acidic environment during reproductive years provides protection against a variety of STPs, so variables that alter the pH predispose a woman to infection |
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Antibiotics and vaginitis
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antibiotics often destroy normal vaginal flora, facilitating overgrowth of C. albicans, causing a yeast vaginitis
|
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What is one thing that can cause all 4 female 'itis?
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STP's..or sexually transmitted pathogens, that can cause STD's, STI's, risk for infection
|
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What might you see with vaginitis?
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change in pH
swelling itching discharge change |
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What is cervicitis?
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cervicitis is a nonspecific term used to describe inflammation of the cervix prior to the identification of pathogens
|
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Cerviticitis is usually...
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secondary to vaginitis: moves to cervix via mucous membrane, close to each other, nothing structurally separating
|
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Cervicitis clinical manifestations
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exudate from cervical Os (opening)-often painful
friable pain-bleeding easily during sex or pelvic exams and Pap smears |
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Vulvovestiulitis aka..what is it?
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vulvovestibulitis (VV)
aka.. vulvitis vesitbulitis vulvodynia inflammation of the vulva or vestibule of the genitalia, or both fairly common, 10% of women sometime in their life |
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Causes of vulvovestiulitis?
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-irritants..soaps, tight clothes, etc (contact dermatitis)
-candida -STPs -abnormalities in mucosae, muscle, pain pathways |
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Clinical manifestations of vulvovestiulitis?
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irritation
pain swelling |
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Bartholinitis? What is it?
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Bartholinitis, or bartholin cyst, is an inflammation of one or both of the ducts that leads from the introitus (vaginal opening) to the Bartholin glands
|
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Causes of bartholinitis?
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usually microorganisms that infect the lower female reproductive tract
ie Strep/Staph STPs |
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manifestations of bartholinitis?
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duct gets plugged, inflammation and blockage
pain/swelling cyst develops |
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Cervical CA: incidence? prevalence?
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Incidence highest in women 35-44
rates declining since 1970's, d/t pap smear prevalence, finding changes in cervix earlier 1 in 147 women..so get your pap |
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Cervical CA: endocervical columnar epithelium, zone: what are squamous cells?
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Along columnar epithelium, can see lighter pink cells that are made of squamous (square) cells
-exocervical (further away from Os) |
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Cervical CA: cervical os, zone: what are glandular cells?
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can see darker red area made up of glandular cells?
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Cervix? What is the normal border b/w squamous cells and glandular cells called?
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The border is called the transformation zone
|
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Is the border normal?
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-yes, it is normal, moves with age, hormones, pregnancy, pill, etc
-moves either out or in, occurs d/t change in cell -changes from metaplasia (change b/w cells), change in squamous to columnar and maybe back |
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Where does cervical CA often occur?
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-often occurs around transformation zone/border
-maybe b/c a lot of genes change there and there is an increased loss of genetic control of cell (basically what CA is) |
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Probably cause of cervical CA..
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HPV
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Cervical CA and HPV..infection in 20's
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In 20's: immune system usually stops progression, even if HPV is present, no need to test for HPV if <30
-controversial guidelines, test is painful so why bother in 20s |
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What HPV strains often cause cervical CA?
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16
18 |
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general patho of cervical CA
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HPV infx (types 16, 18, about 15 others..)
--> inflammation of cervix (immune system may resolve infx, if not..) --> dysplasia (disorganized cell growth) --> cervical CA in situ (full thickness of cervical epithelial) --> invasive cervical CA (beyond cervical epithelial, dysplasia moved beyond membrane) |
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Cytology report for cervical CA: least troublesome to most troublesome
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Atypical Squamous Cells:
ASC-US (just means inflammation, atypical squamous cell of undetermined significance) ASC-H LSIL (aka CIN I-II) (LSIL means mild dysplasia, low-grade squamous intraepithelial lesion, potentially CIN I/II, moderate to severe dysplasia) HSIL (Cervical Cancer In Situ (CIS), full thickness of cervical epithelial), corresponds to CIN III (CIN is cervical intraepithelial neoplasia)-moderate to severe dysplasia and CIS Invasive cervical CA ((beyond cervical epithelial) |
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What corresponds to CIN 3? with cervical CA?
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severe dysplasia and CIS
HSIL all or most of the cervical epithelium shows cellular features of carcinoma, but underlying tissue is not affected |
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What is CIS?
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cervical carcinoma in situ (full epithelial thickness of the cervix is involved)
|
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Continuum of cervical CA
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cervical intraepithelial neoplasia (dysplasia)
to... cervical carcinoma in situ to.. invasive carcinoma (dysplasia now moved beyond basement membrane) |
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starred in notes..number of people who dx with cervical CA and died in 2009
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Dx (incidence): 12,200
Died: 4,210 |
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Cervial CA risk factors
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-HPV
-multiple partners (b/c increases HPV risk) -smoking -immunosuppression (risk for progression of HPV) -chlamydia -diet low in fruit/veggies -OCP for cumulative 5+ yrs -multiple pregnancies 3+ -poverty -family hx |
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Cervical CA screening guidelines
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Controversial....
-Age 21 regardless of age at first sexual encounter (No HPV-DNA testing) -Age 21-29 q2yrs (if 3 consecutive normal tests) -Age >30 q3yrs (if 3 consecutive nml tests and consistency with partner, include HPV/DNA test) -Age >65-70 stop (if 3 consecutive nml test and no abnml in past 10 yrs) -screen more frequently if necessary -schedule is the same if umminized |
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ovarian CA stats, starred in ppt
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-2009 incidence: 21,550
-2009 death: 14,600 -more common than cervical CA -incidence increases with advancing age |
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two major types of ovarian cancer?
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epithelial ovarian neoplasms and germ cell neoplasms
-most ovarian malignancies are epithelial ovarian neoplasms that usually develop from the surface epithelium of the ovary or that which line cysts immediately beneath the ovarian surface, usually arise from a single cell, can be malignant, benign, or borderline malignant -germ-cell tumors: derived from the primitive germ cells (gametes) of the embryonic gonad and may be malignant or benign |
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Are germ cells aggressive in ovarian cancer?
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yes, rare but aggressive
|
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How do neoplasms turn to cancer in ovarian cancer?
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we don't know, but epithelial malignancy is the most common
|
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Subcategories of epithelial neoplasm: benign and borderline malignant
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can either be..
1) Serous Adenomas 2) Mucinous Adenomas |
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Subcategory of epithelial neoplasm: malignant..
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can be
1) Adenocarcinomas 2) Serous Epithelial Malignancy |
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Ovarian cancer-risk factors
|
age
obesity no pregnancy (pregnancy and OCP lowers risk) fertility drugs family hx (breast CA- BRCA1 and BRCA-2 mutations), ovarian CA, colon CA -personal breast CA -high fat diet -CV issues |
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ovarian CA screening
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tough one..no great screen method
-NOT pap!!! cervix, not ovaries -u/s-possible, may or may not see change in ovaries, and is expensive and uncomfy when transvaginal.. -BRCA1 and BRCA2-possible, but doesn't necessarily mean you have breast or cervical CA -CA-125-but not conclusive..other things can cause increase -possible CAT scan.. |
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Men's health
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men's health..who cares
|
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Male -itis
4 discussed in class |
urethritis
orchitis epididymitis prostatitis |
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Urethritis in men-what is it?
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urethritis is an inflammatory process of the urethra without concurrent bladder infection that is usually, but not always, caused by a STP
|
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Causes of urethritis in men?
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STPs
inflammation (i.e. from foreign body, foley, or inserting something odd) |
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clinical manifestation of urethritis in men
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irritation to pain
discharge |
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orchitis-what is it?
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orchitis is an acute inflammation of the testes and is uncommon except as a complication of systemic infection or as an extension of an associated epididymitis
|
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orchititis causes
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systemic infection (via blood/lymph or from mumps virus)
epididymitis |
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clinical manifestation of orchitis
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s/sx of systemic infection
edema pain sterility!! |
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What is epididymitis?
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inflammation of the epididymis (a curved structure at the back of the testicle in which sperm matures and is stored), generally occurs in sexually active young males (younger than 35) and is rare before puberty
|
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Causes of epididymitis?
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-acute bacterial (ascending UTI, unprotected sex, anal sex/E Coli)
-chronic bacterial infection (recurrent) -nonbacterial (inflammation, reflux of sterile urine) |
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Clinical manifestations of epididymitis?
|
pain
urinary changes urinary obstruction |
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What is testicular tortion? timeline?
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EMERGENCY in neonates and pubertal adolescents but can occur at any age
-rotation of a testis, which twists blood vessels in the spermatic cord -can lose testicle -sx tx w/in 6 hrs-testicle can be saved 90% of the time -tx after 24 yrs-only 10% |
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patho of testicular tortion?
|
twisting of sematic cord
--> decreased blood flow --> ischemia --> loss of testicle |
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causes of testicular tortion?
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physical exertion, trauma, can occur spontaneously..
|
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clinical manifestations of testicular tortion?
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N/V
dizziness PAIN not relieved by support, rest etc. |
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Assessing the prostate
|
difficult b/c in rectal exam you can only touch on 1 side
-but it's multidimensional -can feel inflammation or mass on just 1 side of the prostate |
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What is the prostate gland?
|
secretory gland, composed of alveoli and ducts embedded in fibromuscular tissue
-while semen moves thru the prostatic portion of the urethra, the prostate gland contracts rhythmically and secretes prostatic fluid into the mixture |
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Prostate histology
|
epithelial cells
stroma cells (outside) |
|
Testosterone in blood is bound to..
|
sex hormone binding globulin (SHBG)
albumin |
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Testosterone in blood-how much?
|
1-2% free testosterone, enters prostate
|
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Free testosterone in blood goes through..2 initial things
|
1) aromatoase
2) 5 alpha reductase |
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T, E, and prostate, what happens after free testosterone goes thru aromatase?
|
ezyme changes --> estrogen
|
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T, E, and prostate, what happens after free testosterone goes through 5 alpha reductase?
|
5 alpha reductase changes T --> DHT (dihydrotestosterone)
---> breakdown into --> AAG |
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T, E, and prostate, what else does DHT do?
|
as well as breakdown into AAG...
DHT ---> activates.. enzymes that regulate intracellular androgens |
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Aging, T, E, and the prostate: basics
|
Environment with increased estrogen and the same or less testosterone
..imbalance |
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Aging, T, E, and the prostate specifically epithelial cells
|
Epithelial cells with aging prostate:
1) decreased 5 alpha reductase 2) decreased DHT |
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Aging, T, E, and the prostate: stroma cells
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stroma cells (outside)
1) increased estrogen 2) 5 alpha reductase and DHT remain the same |
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Benign Prostatic Hyperplasia/hypertrophy: frequency
|
increased frequency with increased age
-60%-70% = 1/2 ->70=90% |
|
BPH simple two causes
|
1) hyperplasia (increase of cell numbers) of nodules
2) hypertrophy (increase in cell size) of glandular cells both lead to nodules |
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main sx of BPH and questions to ask
|
-urinary changes if frequent sx
-"Could you write your name in the snow?" if no, decreased force of stream, possible sx -"How many times do you get up at night to use BR" if several, possible sx |
|
BPH: patho
|
testosterone
--> 5 alpha reductase --> DHT --> enlarged prostate -estrogen may sensitize prostate tissue to DHT -changed balance of DHT in epithelial and stromal cells promote growth and tissue changes -other growth simulation and inhibition factors? |
|
nodules in prostate
**STARRED** |
nodular changes consistent throughout prostate in normal prostate, not in prostate CA
|
|
prostate CA-stats **STARRED** numbers
|
2010 Incidence: 217,730
2010 Deaths: 32,050 highest incidence in men 55-74 -man's risk of developing prostate CA is 1 in 6 |
|
Prostate CA: what leads to inflammation of prostate?
|
1) environmental agents: diet, infection, smoking
2) urinary reflux |
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Inflammation of prostate leads to?
|
oxidative stress - estrogen generated?
-oxidation may be r/t increased estrogen in r/t testosterone |
|
oxidation leads to
|
prostatic intraepithelial neoplasm (PIN)
|
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Pin leads to..
|
prostate CA
-but not everybody with PIN gets prostate CA and some with prostate CA don't have PIN |
|
prostate CA-risk factors
|
-age
-race/ethnicity A.A. increased -nationality -family hx -genetics -diet -smoking -vasectomy |
|
prostate CA-screening
|
-start at age 50: 45 in A.A. or family hx
-Tests: digital rectal exam; Prostate-Specific antigen (PSA) >4; Biopsy |
|
Is PSA a great test?
|
no, can increase b/c of BPH, or no reason at all
-can also have prostate CA without PSA -increase-recommendation is biopsy-but even a biopsy may not hit the lesion, may get normal result -prostate CA is slow growing CA |
|
Is DRE a great test?
|
can only feel it on one side, so no
|
|
Prostate CA vs BPH:
areas of induration, rank, nodules on DRE? |
CA: yes
BPH: no |
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Prostate CA vs BPH: symmetrical enlargement, firmness of the prostate?
|
CA: no
BPH: yes |
|
Prostate CA vs BPH: nocturia, urinary frequency, urgency, hesitancy?
|
CA: possible in advanced CA
BPH: more likely yes |
|
Prostate CA vs BPH: erectile dysfunction?
|
CA: in advanced CA
BPH: increased incident with BPH |
|
Prostate CA vs BPH: hematuria, hematospermia
|
CA: uncommon
BPH: possible if UTI |
|
Prostate CA vs BPH: bone pain?
|
CA: metastatic disease in small percentage
BPH: no |
|
Sexual dysfunction: female:
|
vaginismus
painful intercourse orgasmic dysfunction |
|
sexual dysfunction: vaginismus
|
involuntary contraction of vagina, can be psychological, lack of desire
|
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sexual dysfunction: female painful intercourse
|
pain-can be size of organ, vag too small, psychological, decreased lubrication,
-can be low estrogen, maybe perimenopausal -structural-changes in vagina, position may change (be graphic, ask questions, does it hurt on top, underneath) |
|
sexual dysfunction: female orgasmic dysfunction
|
-unable to achieve orgasm
-obviously women don't always orgasm sex -may be b/c of trauma, depression, libido, hormones |
|
sexual dysfunction: men-erectile dysfunction
|
-unable to achieve/maintain erection
|
|
sexual dysfunction-men- ejaculation:
|
-ejaculation-decreased testosterone, could be neurological-innervation/paralysis, back issue nerve pressure, psychological
|
|
sexual dysfunction-psychological
|
bad experience sexually, may be fear of next one being one, see a sexual counselor
|
|
sexual dysfunction-desire
|
libido
-psychological-fear, present/past trauma, negative experience, upbringing -organic-drug use, low testosterone can interfere with libido |
|
sexual dysfunction: health of organs
|
-need organs that aren't too dry, ie vagina
-need erect penis -infection, neurologic changes |
|
sexual dysfunction-systemic health
|
-fatigue
-anxiety -depression -CV -DM -infection: ie PID may make intercourse too painful -neuro-ie paralysis may make it impossible to erect |
|
Infertility: what it is?
|
no conception for 1 year with unprotected intercourse with the same partner
|
|
Infertilit:L structure
|
all organs must be present, patent, healthy, tubes open
|
|
Infertility: function
|
-endocrine
-gamete formation-ie ovary follicle and ovulation -support of sperm-seminal fluid supports sperm, needs to be right viscosity (certain drugs/toxins hurt this); -antibodies must not be present against man's sperm (both sexes can have this) -support of pregnancy-need uterus that can accept/support fertilized egg and carry pregnancy |
|
Female reproductive system: hormones
1) hypothalamus releases.. |
1) Hypothalamus releases GnRH
|
|
Female reproductive system: hormones
2) GnRH goes to.. |
GnRH goes to anterior pituitary
|
|
3) Female reproductive system: hormones: From anterior pituitary..what gets released
|
Anterior pituitary releases FSH and LH
|
|
4) Female reproductive system: hormones
FSH does what? LH does what? |
Ovaries:
FSH forms follicle LH produces ovulation |
|
5) What happens after follicle formation
What happens simultaneously |
In ovary..simultaneously
Follicle formation releases estrogen to uterus Corpus Luteum releases estrogen and progesterone to uterus |
|
Male reproductive system-hormones:
1) First step |
Hypothalamus releases GnRH
|
|
Male reproductive system-hormones:
2) what happens after GnRH |
2) GnRH goes to antior pituitary
|
|
Male reproductive system-hormones:
3) what happens after the anterior pituitary |
3) FSH and LH released
|
|
4) Male reproductive system-hormones: What happens after FSH and LH
|
4) In testes
FSH go to Sertoli Cells LH goes to Leydig Cells |
|
5) What happens after Sertoli Cells and Leydig Cells?
|
Sertoli Cells --> Spermatozoa
Leydig Cells --> Testosterone |
|
Delayed puberty what is it?
|
Late puberty
-no signs of puberty by 13 for girls -no signs of puberty by 14 for boys |
|
Causes of delayed puberty?
|
In 95% of cases..
-hormonal levels are nml -the hypothalamus-pituitary-gonadal axis is intact -but maturation is happening slowly -familial tendency and more common in boys -can be f/ chronic condition that delays bone development and aging -exogenous sex steroid administration is used to reduce embarrassment |
|
What is precocious puberty?
|
early sexual maturation
-before 6 in white girls -before 7 in black girls -before age 9 in boys |
|
What is central precocious puberty?
|
Gn-RH dependent and occurs when the hypothalamic-pituitary-gonadal axis is functioning normally but prematurely
|
|
What is peripheral puberty?
|
is GnRH independent and develops when sex hormones are produced by some mechanisms other than stimulation by the gonadotropins
-some causes are gonadal tumors, testotoxicosis, and exposure to exogenous sex steroids |
|
What is endometriosis?
|
the presence of functioning endometrial tissues or implants outside of the uterus
-ectopic (out of place) endometrium responds to the hormonal flunctuations of the menstrual cycle |
|
endometriosis and cancer?
|
increased risk of some cancers
|
|
endometriosis cause?
|
not known, some theories:
-retrograde menstruation: menstrual fluids move thru the fallopian tubes and empty into the pelvic cavity, occurs in almost all women -impaired cellular and humoral immunity -autoimmune response, body can tolerate ectopic implantation of endometrial cells -genetic predisposition |
|
Where does endometriosis usually occur?
|
endometrial implants can occur anywhere, but usually in pelvic and abdominal cavities
|
|
Clinical manifestations of endometriosis?
|
-ectopic endometrium proliferates, breaks down, and bleeds in conjunction with the normal menstrual cycle
-the bleeding causes inflammation -infertility and pain, dysmenorrhea, dyschezia (pain defecation) -pelvic mass/nodules |
|
STI's-it is common to have..
|
STI's common to have multiple STI's
-infection with one STI increases the risk for additional STIs |
|
STI's maternity
|
-the microbes that cause STIs can spread from pregnant women to the fetus potentially causing severe damage to the fetus or child
-STIs can cause getting/maintaining pregnancy problematic |
|
Bacterial Vaginosis-what is it?
-Is it an STI? associations |
overgrowth of bacteria that shouldn't be there
-STI? Kind of..not really -can get it w/o sexual contact -occurs most often in sexually active women, often with a new partner..maybe -douching can also cause, it is cultural to some ppl but not health |
|
Bacterial Vaginosis-one organism in particular..
|
A DECREASE in Lactobacilli = environment for other organisms
-Lactobacilli should be there, if decreased sets the stage for other bacteria to come in |
|
Bacterial vaginosis-symptoms
|
-copious thin, malodorous discharge
-high vaginal pH of 5-5.5 -clue cells: darker, spotty speckles, bacteria, thickening of cell border as opposed to normal vaginal epithelial cells |
|
Bacterial Vaginosis effects
|
-PID, prego complications
|
|
Bacterial Vaginosis tx
|
tx doesn't help, same recurrence/relapse rate
|
|
Gonorrhea & CHlamydia often occur..
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gonorrhea and chlamydia often occur together, but they are different
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gonorrhea organism-what is it?
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Neisseria gonorrhoeae
-aerobic, gram -diplococci with pill |
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chlamydia organism
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Chlamydia trichomatis
-aerobic, gram -cocci -obligate to host for ATP needed for replication |
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What is a big difference b/w gonorrhea and chlamydia?
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chlamydia needs a host organism to replicate
gonorrhea can replicate on its own |
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What does gonorrhea infect?
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columnar, transitional, and epithelial cells
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What does chlamydia infect?
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squamous, columnar, and epithelial cells?
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What happens during gonorrhea infection?
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-adheres to plasma membranes of host cell
-invades cell -quick immune response - inflammation! |
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What happens during chlamydia infection?
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-has elementary body that attacks cells
-attaches to a host cell and enters -uses host's ATP for replication inside host -host cell lyses = new elementary bodies released |
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Gonorrhea and chlamydia sx..
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may not have any, especially in women
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Gonorrhea incubation
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3-10 days for gonorrhea incubation, possibly longer
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Chlamydia incubation
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chlamydia incubation 7-21 days
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Gonorrhea sx:
men |
Gonorrhea sx for men:
-sudden dysuria, mucopurulent discharge (not clear) |
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Gonorrhea sx women
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Gonorrhea sx women
-dysuria, discharge, friable cervix |
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Gonorrhea/Chlamydia sx both sexes
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-rectal: anal pruitis/itching, mucopurulent rectal discharge, pain
-oral: pharangitis -eye: conjunctivitis |
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Chlamydia sx men
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men chlamydia: dysuria, clearer discharge, mucous discharge
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Chlamydia sx women
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mucopurulent discharge from cervix, friable cervix
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Chlamydia symptom..
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"the drip" for men, crusting in underwear, clear-er discharge
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Both Gonorrhea and Chlamydia have ___ as a complication for men and ___ as a complication for women
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Gonorrhea & Chlamydia
Men complication: epidydymis Women complication: PID |
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Gonorrhea: complication in both men and women
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-disseminated gonoccocoal infection (DGI)..think G
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Chlamydia: complication for both men and women
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-Reiter syndrome: type of arthritis-inflammation/soreness in joints
-conjunctivitis |
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Newborn complications with gonorrhea
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Blindness
-opthalmia neonatorum -increased risk longer membranes are ruptured -can cause blindness |
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Chlamydia newborn complication
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-pneumonia
-also opthalmia neonatorum |
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Pelvic Inflammatory Disease: what is it?
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infection of female upper reproductive track
-uterus, fallopian tubes (salphinigitis), ovaries (oophoritis) |
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PID causes
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-lots of organisms can cause it
-columnar epithelial cell changes (i.e. f/ G/C) causes environment vulnerable to bacteria -movement of bacteria into upper organs -i.e. overgrowth of vag, Male reproductive system-hormones: thru lymphs, infx sperm swim to uterus, menstruation open to endocervical canal, contraction of uterus movement into uterus (retrograde menstruation) |
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PID sx
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-PAIN-hospitalized sometimes
-risk of scarring, scar tissue -decreased fertility risk -cervical motion tendenress-when 2 fingers into vag and push against cervix/uterus pain |
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Syphilis organism
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Treponema pallidum
-anaerobic -spirochaetes |
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Syphilis occurs in different..
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stages
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Primary syphilis stage
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primary syphilis stage is where infx bacteria enters
Chancre: -sore on epithelium -onset 10-90 days after exposure -duration: 2-8 weeks of shanker -lymphadenopathy -contagious -lymph and then... |
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Secondary syphilis stage
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infection on epithelium --> travels through lymph --> travels through system --> this is when it's secondary syphilis
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When does secondary syphilis occur?
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about 6 weeks after chancre
systemic-all organ systems |
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Sx of syphilis: skin
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Rash
-bilateral palms and plantar surface of feet -can be other locations -condylomata lata (wart like lesions) |
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Sx of secondary syphilis-oral cavity
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Oral cavity
-mucous patches |
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Secondary syphilis: other sx
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-flu like symptoms
-lymphadenopathy, pruititis, ESR, hepatitis, proteinuria, arthritis |
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Is secondary syphilis contagious?
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Yes
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Whend oes secondary syphilis resolve?
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resolves in 2-10 weeks
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Latent syphilis is categorized by?
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-resolution of stage 1 and 2
-no symptoms but still infected -may remain in latent stage for rest of life -contagious! Some may progress to.. |
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Tertiary syphilis-when does it occur? Contagious?
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Some remain in latent stage for life, others progress to tertiary stage
-after 5+ years of latency No longer "as" contagious-transmission rate 10% -transmission is just contact w/ shanker |
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Tertiary syphilis- CV syphilis
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-CV Syphilis
-dilation of aortic root and arch -aortic valve insufficiency and aneurysm |
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Tertiary syphilis- Neurosyphilis
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-Neurosyphilis
-meningovascular disease, generalized brain parenchymal disease, CSF abnormalities, increased number inflammatory cells, increased protein levels, decreased flucose, antibodies to spirochetes |
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Tertiary syphilis-benign tertiary syphilis
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-Benign Tertiary Syphilis
-gummas (lesions caused by noninflammatory tissue necrosis) |
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What is congenital syphilis?
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transmission occurs in utero or during birth
-often stillborn, death shortly after delivery, or usually within first 2 years |
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Congenital syphilis-early sx
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Early sx-newborns
-failure to gain weight -fever -irritability -no bridge to nose -early rash-small blisters on the palms and soles -later rash-copper-colored, flat or bumpy rash on the face, palms, and soles -rash of mouth -genitalia and anus rash -water discharge of nose |
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Congenital syphilis-later sx
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Congenital sx-older infants
-abnormal notched and peg shaped teeth -bone pain -blindness -clouding of the cornea -decreased hearing or deafness -gray mucus like patches on the anus and outer vagina -joint swelling -refusal to move a painful arm or leg -scarring of the skin around the mouth, genitalia, or anus |
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Herpes Simplex Virus-two strains
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2 strains are HSV-1 and HSV-2
-both can either affect mouth or genetalia -likes to affect mucus tissue |
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Herpes Simplex Virus-incubation
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2-10 days
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Herpes Simplex Virus- genetic
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encapsublated, double stranded DNA
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Herpes Simplex Virus- transmission
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-from: infected secretions, lesions, mucosa
-To: uninfected mucocutaneous tissue or abraded skin -enters via mucus membrane --> moves to innervating sensory nerve --> moves to dorsal nerve |
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Herpes Simplex Virus- first step
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Entry: HSV enters the body through skin or mucus membrane
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Herpes Simplex Virus- second step
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Latency:
After initial infection, HSV settles in nerves near the spine -Latency-hangs out in nerve root, nerve can replicate and cause recurrence, can have multiple recurrences or rare, varies based on stress, health |
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Herpes Simplex Virus- Two next steps:
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-Recurrence: HSV travels along the nerves, back to the skin to form new blisters
-Asymptomatic viral shedding: HSV travels along the nerves, back to the skin, but does not form new blisters |
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HSV tends to hang out in..
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oral: trigeminal nerve
Genital: Sacral nerve |
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HSV: Primary First episode..
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Primary:
-3 days-2 weeks after exposure -asymptomatic -systemic-may feel sick/flu like -lesions-last 10-20 days |
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HSV non--primary first episode
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-? when
-systemic -lesions |
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HSV-Recurrent
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Recurrent:
-? when -lesions: 4-5 days, often prodromal sx -When does it occur? depends -often have burning/itching when it's about to come, i.e cold sores -looks like blisters -can be transmitted to newborn via birth canal in delivery |
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HPV genetic
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-nonenveloped, double stranded DNA virus
-very common! 75% of reproductive age |
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HPV -STD?
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-considered STD but some may get it w/o sexual cotact
-virus may not show itself right away, latent incubation period can be very long -high risk strains and low risk strains |
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HPV linked to..
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cervical CA-high risk strains
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Human Papillomavirus (HPV)-how does it infect?
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break in epithelium --> can infect basal cells of epithelium and cause infection
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HPV manifestations 2-3 months
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-cervix-inflammation, dysplasia, etc.. with high risk strains
-Other structures: condylomata acumina with low risk types (contagious warts) |
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Cure for HPV?
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-no cure
-Gardasil vaccine, controversial b/c only covers 2 high risk and 2 low risk strains -false sense of security -to see hpv coloscopy of cervix, vinegar on cervix and infx tissue looks white |
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Trichomoniasis-what is it?
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infection of T. vaginalis - parasitic infection
-T. vaginalis is a parasitic protozoan that adheres to and damages squamous epithelial cells -often coexists with gonorrhea |
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Trichomoniasis-what is trichomonads?
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-the protozoa
-self limiting inmen b/c prostate has potent antibacterial Zinc -most infxs of the male urethra clear up w/in 2 weeks -primarily infx of the vagina |
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Manifestations of trichomoniasis
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-range from none to severe
-discharge, vaginal pruritis, dysparareunia and dysuria -secretions are copious, frothy, malodorous, and gray-green -rarely, small red puncture marks called strawberry spots |
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Tx for trich
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single dose Flagyl
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What is pediculosis pubis?
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the crab louse, one of three species of lice that infest humans, "crabs"
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pediculosis pubis transmission? who gets affected?
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-most common among kids and adolescents
-transmitted via sex, bed linens, clothes -pubic lice, also other hair on body |
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pediculosis pubis? patho
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-crabs are "glued" to hairs, cling to pubic hairs
-depend on blood for nutrition, they bite into skin to obtain food -3 stages 1) egg nit stage 2) three nymphal stages 3) adult stage -all occur on host |
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Clinical manifestations pediculosis pubis?
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-range from mild pruritis to severe, intolerable itching, depeding on sensitivity to bite
-allergic senstiization occurs in about 5 days -excessive scratching..secondary infection |
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pediculosis pubis tx
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cream, lotion with permethrin cream or lindane lotion 1%
-repeat in 7 days for newly hatched eggs |