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234 Cards in this Set

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The menstrual cycle..bleeding and fertile times
28 day cycle
Day 1-5 bleeding
Day 11-15 fertile
For proper menstruation..need proper function of...(brief)
proper function of
hypothalmus
pituitary gland
uterus
10 Steps: Menstrual Cycle Step 1
1. The hypothalamus releases GnRH (Gonadotropin‐
Releasing Hormone).
Menstrual Cycle Step 2
2. The pituitary secretes FSH and LH.
Menstrual Cycle Step 3
3. The FSH and LH stimulate follicle growth.
Menstrual Cycle Step 4
4. The follicles start to make estradiol. Several follicles
begin to grow with each cycle, but usually only one matures.
Menstrual Cycle Step 5
5. Around day 12 estradiol levels rise steeply.
Rising estradiol stimulates a LH surge by positive feedback.
Menstrual Cycle Step 6
6. The LH surge triggers ovulation: the follicle ruptures,
releasing the secondary oocyte.
Menstrual Cycle Step 7
7. The follicle left in the ovary forms the corpus luteum,
which secretes progesterone and estradiol.
Menstrual Cycle Step 8
8. Rising progesterone and estradiol levels stimulate
thickening of the uterine wall, or endometrium.
Menstrual cycle-Step 9
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.
Menstrual cycle-step 10
10. This continues for about 450 cycles, then women enter menopause.
Dysfunction of menstrual cycle: what is painful period?
dysmenorrhea
Subcategories of dysmenorrhea: first one
primary and secondary
primary: painful menstruation associated with the release of prostaglandins in ovulatory cycles, but not with pelvic disease, no other cause identified
Subcategories of dysmenorrhea: secondary
Secondary: pelvic pathology
i.e. IUD, PID, endometriosis
What are some common causes of primary dysmenorrhea?
-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
Amenorrhea: difference between two categories
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
Primary amenorrhea: 4 categories of causes
1) hypothalamus
2) ovary
3) anterior pituitary
4) uterus/vagina

..primary amenorrhea usually r/t issues of structures or hormones
Primary amenorrhea: break down causes of hypothalamus
Primary Amenorrhea: hypothalamus causes:
-No GnRH release
Primary amenorrhea: break down of causes from Ovary
Primary Amenorrhea f/ ovary:
-no ovaries
-no gametes
-no follicle/follicular development
-no estrogen release
Primary Amenorrhea: anterior pituitary causes
-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
Primary Amenorrhea: uterus/vagina causes
-absent uterus and/or vagina
-infantile uterus
2 syndromes possibly r/t primary amenorrhea
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
Secondary amenorrhea: general list of causes
Hypothalamus
Ovary
Anterior Pituitary
Uterus
Secondary amenorrhea: patho from high prolactin
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
secondary amenorrhea: hypothalamus causes
-decreased GnRH release
-structural change
-elevated prolactin
-elevated estrogen and progesterone (i.e. from pregnancy, the pill, stress, weight loss, excessive exercise)
Secondary amenorrhea: ovary causes
-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
Secondary amenorrhea: ovary causes..relationship b/w E/P and GnRH
-oversecretion of E/P --> inhibits GnRH
-undersecretion of E/P ---> doesn't respond to GnRH
Secondary amenorrhea: anterior pituitary causes
-decreased FSH/LH
-structural cause
Secondary amenorrhea: uterus causes
-hysterectomy
-endometrial ablation or adhesions
Most common causes of seondary amenorrhea
-pregnancy
-hypothyroidism (assoc w/ high prolactin)
-hyperprolactinemia
-HPO interruption secondary to excessive exercise, stress, weight loss, and PCOS
Abnormal Uterine bleeding-how is it dx?
dx of exclusion: look for fibroids, polyps, clotting, infection, pregnancy, ovarian cysts, bleeding d/o
abnormal uterine bleeding-what is it?
heavy or irregular bleeding in the absence of organic disease, such as submucous fibroids, endometrial polyps, blood dyscrasias, pregnancy, infx, or systemic disease
Is abnormal uterine bleeding common?
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
What are some chronic conditions that can cause or are assoc w/ abnml uterine bleeding?
-chronic conditions
-adrenal conditions
-thyroid d/o
-liver disease
-DM
-obesity
-HTN
What is a common cause of abnormal uterine bleeding in perimenopausal women? patho
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
abnormal uterine bleeding in postmenopausal women?
postmenopausal women 1 year after cessation of periods-worry about malignancy, concern
What is a normal vaginal pH?
3.8 - 4.8
What condition is often caused by disruption in vag pH? Implications for too high? Too low?
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
What are the 4 female -itis talked about in class?
Bartholinitis
Vulvo-vestibiulitis
Vaginitis
Cervicitis
How is pH of vag regulated? What is its purpose
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
Antibiotics and vaginitis
antibiotics often destroy normal vaginal flora, facilitating overgrowth of C. albicans, causing a yeast vaginitis
What is one thing that can cause all 4 female 'itis?
STP's..or sexually transmitted pathogens, that can cause STD's, STI's, risk for infection
What might you see with vaginitis?
change in pH
swelling
itching
discharge change
What is cervicitis?
cervicitis is a nonspecific term used to describe inflammation of the cervix prior to the identification of pathogens
Cerviticitis is usually...
secondary to vaginitis: moves to cervix via mucous membrane, close to each other, nothing structurally separating
Cervicitis clinical manifestations
exudate from cervical Os (opening)-often painful

friable pain-bleeding easily during sex or pelvic exams and Pap smears
Vulvovestiulitis aka..what is it?
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
Causes of vulvovestiulitis?
-irritants..soaps, tight clothes, etc (contact dermatitis)
-candida
-STPs
-abnormalities in mucosae, muscle, pain pathways
Clinical manifestations of vulvovestiulitis?
irritation
pain
swelling
Bartholinitis? What is it?
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
Causes of bartholinitis?
usually microorganisms that infect the lower female reproductive tract

ie Strep/Staph
STPs
manifestations of bartholinitis?
duct gets plugged, inflammation and blockage
pain/swelling
cyst develops
Cervical CA: incidence? prevalence?
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
Cervical CA: endocervical columnar epithelium, zone: what are squamous cells?
Along columnar epithelium, can see lighter pink cells that are made of squamous (square) cells

-exocervical (further away from Os)
Cervical CA: cervical os, zone: what are glandular cells?
can see darker red area made up of glandular cells?
Cervix? What is the normal border b/w squamous cells and glandular cells called?
The border is called the transformation zone
Is the border normal?
-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
Where does cervical CA often occur?
-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)
Probably cause of cervical CA..
HPV
Cervical CA and HPV..infection in 20's
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
What HPV strains often cause cervical CA?
16

18
general patho of cervical CA
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)
Cytology report for cervical CA: least troublesome to most troublesome
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)
What corresponds to CIN 3? with cervical CA?
severe dysplasia and CIS

HSIL

all or most of the cervical epithelium shows cellular features of carcinoma, but underlying tissue is not affected
What is CIS?
cervical carcinoma in situ (full epithelial thickness of the cervix is involved)
Continuum of cervical CA
cervical intraepithelial neoplasia (dysplasia)

to...

cervical carcinoma in situ

to..

invasive carcinoma (dysplasia now moved beyond basement membrane)
starred in notes..number of people who dx with cervical CA and died in 2009
Dx (incidence): 12,200

Died: 4,210
Cervial CA risk factors
-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
Cervical CA screening guidelines
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
ovarian CA stats, starred in ppt
-2009 incidence: 21,550
-2009 death: 14,600

-more common than cervical CA
-incidence increases with advancing age
two major types of ovarian cancer?
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
Are germ cells aggressive in ovarian cancer?
yes, rare but aggressive
How do neoplasms turn to cancer in ovarian cancer?
we don't know, but epithelial malignancy is the most common
Subcategories of epithelial neoplasm: benign and borderline malignant
can either be..

1) Serous Adenomas

2) Mucinous Adenomas
Subcategory of epithelial neoplasm: malignant..
can be

1) Adenocarcinomas

2) Serous Epithelial Malignancy
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
ovarian CA screening
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..
Men's health
men's health..who cares
Male -itis
4 discussed in class
urethritis
orchitis
epididymitis
prostatitis
Urethritis in men-what is it?
urethritis is an inflammatory process of the urethra without concurrent bladder infection that is usually, but not always, caused by a STP
Causes of urethritis in men?
STPs
inflammation (i.e. from foreign body, foley, or inserting something odd)
clinical manifestation of urethritis in men
irritation to pain
discharge
orchitis-what is it?
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
orchititis causes
systemic infection (via blood/lymph or from mumps virus)
epididymitis
clinical manifestation of orchitis
s/sx of systemic infection
edema
pain
sterility!!
What is epididymitis?
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
Causes of epididymitis?
-acute bacterial (ascending UTI, unprotected sex, anal sex/E Coli)
-chronic bacterial infection (recurrent)
-nonbacterial (inflammation, reflux of sterile urine)
Clinical manifestations of epididymitis?
pain
urinary changes
urinary obstruction
What is testicular tortion? timeline?
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%
patho of testicular tortion?
twisting of sematic cord
--> decreased blood flow
--> ischemia
--> loss of testicle
causes of testicular tortion?
physical exertion, trauma, can occur spontaneously..
clinical manifestations of testicular tortion?
N/V
dizziness
PAIN not relieved by support, rest etc.
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
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
Prostate histology
epithelial cells
stroma cells (outside)
Testosterone in blood is bound to..
sex hormone binding globulin (SHBG)
albumin
Testosterone in blood-how much?
1-2% free testosterone, enters prostate
Free testosterone in blood goes through..2 initial things
1) aromatoase
2) 5 alpha reductase
T, E, and prostate, what happens after free testosterone goes thru aromatase?
ezyme changes --> estrogen
T, E, and prostate, what happens after free testosterone goes through 5 alpha reductase?
5 alpha reductase changes T --> DHT (dihydrotestosterone)

---> breakdown into

--> AAG
T, E, and prostate, what else does DHT do?
as well as breakdown into AAG...

DHT ---> activates..

enzymes that regulate intracellular androgens
Aging, T, E, and the prostate: basics
Environment with increased estrogen and the same or less testosterone

..imbalance
Aging, T, E, and the prostate specifically epithelial cells
Epithelial cells with aging prostate:

1) decreased 5 alpha reductase
2) decreased DHT
Aging, T, E, and the prostate: stroma cells
stroma cells (outside)

1) increased estrogen
2) 5 alpha reductase and DHT remain the same
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
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
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)
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
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
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..
gonorrhea and chlamydia often occur together, but they are different
gonorrhea organism-what is it?
Neisseria gonorrhoeae
-aerobic, gram
-diplococci with pill
chlamydia organism
Chlamydia trichomatis
-aerobic, gram
-cocci
-obligate to host for ATP needed for replication
What is a big difference b/w gonorrhea and chlamydia?
chlamydia needs a host organism to replicate

gonorrhea can replicate on its own
What does gonorrhea infect?
columnar, transitional, and epithelial cells
What does chlamydia infect?
squamous, columnar, and epithelial cells?
What happens during gonorrhea infection?
-adheres to plasma membranes of host cell
-invades cell
-quick immune response - inflammation!
What happens during chlamydia infection?
-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
Gonorrhea and chlamydia sx..
may not have any, especially in women
Gonorrhea incubation
3-10 days for gonorrhea incubation, possibly longer
Chlamydia incubation
chlamydia incubation 7-21 days
Gonorrhea sx:

men
Gonorrhea sx for men:
-sudden dysuria, mucopurulent discharge (not clear)
Gonorrhea sx women
Gonorrhea sx women
-dysuria, discharge, friable cervix
Gonorrhea/Chlamydia sx both sexes
-rectal: anal pruitis/itching, mucopurulent rectal discharge, pain
-oral: pharangitis
-eye: conjunctivitis
Chlamydia sx men
men chlamydia: dysuria, clearer discharge, mucous discharge
Chlamydia sx women
mucopurulent discharge from cervix, friable cervix
Chlamydia symptom..
"the drip" for men, crusting in underwear, clear-er discharge
Both Gonorrhea and Chlamydia have ___ as a complication for men and ___ as a complication for women
Gonorrhea & Chlamydia
Men complication: epidydymis
Women complication: PID
Gonorrhea: complication in both men and women
-disseminated gonoccocoal infection (DGI)..think G
Chlamydia: complication for both men and women
-Reiter syndrome: type of arthritis-inflammation/soreness in joints

-conjunctivitis
Newborn complications with gonorrhea
Blindness
-opthalmia neonatorum
-increased risk longer membranes are ruptured
-can cause blindness
Chlamydia newborn complication
-pneumonia
-also opthalmia neonatorum
Pelvic Inflammatory Disease: what is it?
infection of female upper reproductive track
-uterus, fallopian tubes (salphinigitis), ovaries (oophoritis)
PID causes
-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)
PID sx
-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
Syphilis organism
Treponema pallidum
-anaerobic
-spirochaetes
Syphilis occurs in different..
stages
Primary syphilis stage
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...
Secondary syphilis stage
infection on epithelium --> travels through lymph --> travels through system --> this is when it's secondary syphilis
When does secondary syphilis occur?
about 6 weeks after chancre

systemic-all organ systems
Sx of syphilis: skin
Rash
-bilateral palms and plantar surface of feet
-can be other locations
-condylomata lata (wart like lesions)
Sx of secondary syphilis-oral cavity
Oral cavity
-mucous patches
Secondary syphilis: other sx
-flu like symptoms
-lymphadenopathy, pruititis, ESR, hepatitis, proteinuria, arthritis
Is secondary syphilis contagious?
Yes
Whend oes secondary syphilis resolve?
resolves in 2-10 weeks
Latent syphilis is categorized by?
-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..
Tertiary syphilis-when does it occur? Contagious?
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
Tertiary syphilis- CV syphilis
-CV Syphilis
-dilation of aortic root and arch
-aortic valve insufficiency and aneurysm
Tertiary syphilis- Neurosyphilis
-Neurosyphilis
-meningovascular disease, generalized brain parenchymal disease, CSF abnormalities, increased number inflammatory cells, increased protein levels, decreased flucose, antibodies to spirochetes
Tertiary syphilis-benign tertiary syphilis
-Benign Tertiary Syphilis
-gummas (lesions caused by noninflammatory tissue necrosis)
What is congenital syphilis?
transmission occurs in utero or during birth
-often stillborn, death shortly after delivery, or usually within first 2 years
Congenital syphilis-early sx
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
Congenital syphilis-later sx
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
Herpes Simplex Virus-two strains
2 strains are HSV-1 and HSV-2
-both can either affect mouth or genetalia
-likes to affect mucus tissue
Herpes Simplex Virus-incubation
2-10 days
Herpes Simplex Virus- genetic
encapsublated, double stranded DNA
Herpes Simplex Virus- transmission
-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
Herpes Simplex Virus- first step
Entry: HSV enters the body through skin or mucus membrane
Herpes Simplex Virus- second step
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
Herpes Simplex Virus- Two next steps:
-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
HSV tends to hang out in..
oral: trigeminal nerve
Genital: Sacral nerve
HSV: Primary First episode..
Primary:
-3 days-2 weeks after exposure
-asymptomatic
-systemic-may feel sick/flu like
-lesions-last 10-20 days
HSV non--primary first episode
-? when
-systemic
-lesions
HSV-Recurrent
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
HPV genetic
-nonenveloped, double stranded DNA virus
-very common! 75% of reproductive age
HPV -STD?
-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
HPV linked to..
cervical CA-high risk strains
Human Papillomavirus (HPV)-how does it infect?
break in epithelium --> can infect basal cells of epithelium and cause infection
HPV manifestations 2-3 months
-cervix-inflammation, dysplasia, etc.. with high risk strains
-Other structures: condylomata acumina with low risk types (contagious warts)
Cure for HPV?
-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
Trichomoniasis-what is it?
infection of T. vaginalis - parasitic infection
-T. vaginalis is a parasitic protozoan that adheres to and damages squamous epithelial cells

-often coexists with gonorrhea
Trichomoniasis-what is trichomonads?
-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
Manifestations of trichomoniasis
-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
Tx for trich
single dose Flagyl
What is pediculosis pubis?
the crab louse, one of three species of lice that infest humans, "crabs"
pediculosis pubis transmission? who gets affected?
-most common among kids and adolescents
-transmitted via sex, bed linens, clothes
-pubic lice, also other hair on body
pediculosis pubis? patho
-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
Clinical manifestations pediculosis pubis?
-range from mild pruritis to severe, intolerable itching, depeding on sensitivity to bite
-allergic senstiization occurs in about 5 days
-excessive scratching..secondary infection
pediculosis pubis tx
cream, lotion with permethrin cream or lindane lotion 1%
-repeat in 7 days for newly hatched eggs