GU CM Flashcards
in women of child bearing age abnormal bleeding is attributed to what UNLESS proven otherwise?
PREGNANCY!!!
what test does every woman of child bearing age get when she is having abnormal bleeding?
PREGNANCY TEST!!!
what two tests should ever patient get when they have abnormal bleeding?
- pregnancy test
- CBC with platelets
when you think of dysmennorhhea and infertility in a 25 year old what should you think of?
endometriosis
dismennorreahh and increasing heavy periods in a 48 year old you should think about what two things?
- endometrial hyperplasia/cancer!!! NEED TO THINK OF THIS
regular periods but a uterus the size of a 10 week pregnancy in a 35 year old should make you think of?
a FIBROID!!!
new onset of bleeding in a 70 year old should make you think of?
cancer until otherwise!!
what is the predominat bacterial of the vaginal flora?
lactobacillis
explain the normal vaginal flora and ph of the vagina?
predominant flora?
vaginal wall cell type?
cells make?
pH?
predominant flora: lactobaciillis….produce lactic acid
vaginal wall: strafified squamous
cells make: glyconuitrient rich environment for microorganisms
pH: 3.5-4.5
what are 7 normal organisms in the vaginal canal other than lactobacillis?
- yeast
- e. coli and other fecal bacteria
- garnerella
- staph, strep
- anaerobes
- trichomonads
what should you watch out for if you see discharge in a young woman?
abuse!
where are bartholins glands? what are their function?
two glands located slightly posterior to the left and right of the opening of the vagina
secrete mucous to lubricate the vaginal opening
1 or 2 drops when sexually aroused
what might cause creamy white discharge in 10 year old girl?
early estrogen secretion
what shoud you think of with white vaginal discharge with intense vaginal itching?
yeast!
what should you think of if post coital spotting in a 70 year old woman?
atrophic vaginitis
what should you think about with intense vulvar itiching in a 60 year old?
lichen sclerosis
what should you think of with a asymptomatic mass at the introitus? 2
- bartholin cyst
- relaxation issue
dependent on age as to what to think about!
stress urinary incontinence
who is this common in?
why does it occur?
explain the pressure differences?
what actions might bring this on?
what are 3 things that could cause this in a person?
common problem in women of all ages and results from weakness or disruption in the pelvic floor muscles leading to poor support of the vesicourethral sphincters
usually: the i_ntraurethral pressure is greater than the intravesicular pressure_ which is called the urethral closure pressure
if i_ntra-abdominal pressure increases_ from things like coughing, laughing, or sneezing and the pressure isn’t equally distributed to the urethra then incontinence occurs
causes of decreased muscle tone: aging, child birth, surgical procedures
urge urinary incontinence
what does the pt feel?
what is this associated with?
what is the definition of this?
what are 2 contributing factors?
3 symptoms?
overactive, nocturia, urinary frequency, detrusor overactivity
loss of urine associated with strong desire to void URGENCY, often associated with overactive bladder
definition: urgency, frequency with or without incontinence in the absence of UTI or obvious pathology
Two contributing factors to overactive bladder:
- CNS and neural control of bladder sensation and emptying, ex: stroke, Parkinsons, MS
- smooth muscle of the bladder itself (myogenic)
incomplete emptying “overflow” urinary incontinence
what are 7 signs of this?
what are two causes?
what are 2 causes in women?
what are 2 causes in men?
intravesical pressure exceeds the maximal urethral pressure because of bladder distension
dribbling, weak urinary stream, frequency, and nocturia, hesitancy, frequency, nocturia, nocturnal enuresis (bedwetting), detrusor underactivity or bladder outlet obstruction
women causes: uterine prolapse, previous incontinence surgery
men: most common is enlarged prostate gland
what are the 3 PE tests you want to do with someone with urinary incontinence?
what are the 4 workup tests you would do?
PE:
- pelvic exam
- digital rectal exam (masses, prostate)
- neuro exam if sudden loss (think cauda equina)
Workup:
- urinalysis
- prostate specific antigen
- post void bladder scan
- urology consult
although urinary incontince tx is dependent on the type, what are 5 tx options you could consider?
- fluid management
- timed voiding
- bladder retraining
- keagle/pelvic floor exercises
- surgical intervention
- pessaries to hold uterus up
- decrease caffine/alchohol
- (urge) anticholinergics
(oxybutynin, possibly tricyclic antidepressant)
Nephrolithiasis
what are the two things you need for the formation of crystals?
what are four risk factors that allows this to happen?
what are the four types of stones?
formation is dependent on supersaturation and an environment that allows the stone to grow!
supersaturation risk:
heredity- cystinuria SLC3A1/SLC7A9
environmental
diet
obesity
four types of stones:
- calcium oxalate
- struvite
- uric acid
- cystine
nephrolathiasis
struvite stone
what 2 things is this associated with?
4 bacteria?
can you pass them?
when do they get bigger?
3 tx options?
“staghorn” stones that always associated with UTI and alkaline urine
- produced by UTI with urease producing bacteria
- proteus, klebsiella, pseudomonas, enterobacter
- made of magnesium ammonium
- usually too large to pass and require lithotripsy or surgical removal
- they enlarge as the bacterial count increases
Tx:
- prevent UTIs
- lithrotripsy
- surgical removal
nephrolithiasis
calcium oxalate stones
can you see it on a xray?
what is it usually associated with?
what are 4 associated factors?
3 tx options in general?
MOST COMMON TYPE OF STONE
- RADIOOPAQUE
- usually associated with high calcium levels in the blood and urine
- contributing factors: excessive bone reabsorption, bone disease, hyperparathyroidism and renal tubular acidosis predispose for these stones
TX:
treat underlying conditions
increased fluid intake
thiazide diuretics
(70-80%)
nephrolithiasis
uric acid stone
what is this caused by?
can you see on xray?
what are 2 RF?
2 tx options?
caused by low Ph (acidic) urine
- radiolucent cant be seen on xray
- caused by high levels of uric acid in the urine or gout
- RF: obesity/diabetic or both
Tx:
- decrease uring PH below 6 (more alkaline) using potassium citrate
- allopurinol with decrease purine diet (fish, shellfish, and meats)
nephrolithiasis
cystine stones
what type of disorder is this and who is it common in?
what is the appearance of the stones?
what are the two treatement options?
autosomally recessive inherited abnormalities CYSTINURIA
“childhood caliculi”
1.smooth-edged ground glass appearence
TX:
- increase urine volumes to 3 L a day and increase urine pH to greater than 7
- occasionally chelating agents
what is the most important test when suspecting nephrolithiasis? what do you expect to see for each of the stones? 4 types of labs you should consider ordering?
- non-contrast CT (gold standard)
used to identify the size, location and type of stone
- low density (aka can’t see): uric acid, cystine
- high density: calcium oxalate, struvite
- struvite: laminar, rugged apperance, full of casts with “stag horn apperance”
*****do renal US for pregnant people who can’t have the CT****
- labs
- urinalysis (stone type/blood)
- BMP (calcium and creatinine if worried about kidney function)
- 24 hour urine for the amount excreted
- thyroid function test
what are 6 RF for nephrolithiasis in general?
high humidity
high temp
sedentary
high animal protein and high salt
FH for calcium stones
hyperthyroidism/hypothyroidism
what are the 4 most common symptoms with nephrolithiasis? and less common symtpoms? (4)
Most common:
- unilateral flank pain
- sudden onset
- renal colic
- hematuria
Less common:
- vague abdominal pain
- acute abdominal/flank pain
- difficulty urinating
- penile or testicular pain
what are 6 things that would qualify for urologist referral in a patient with nephrolithiasis?
acute renal failure
urosepsis
urinary obstruction
concomitant pyelonephritis
>10 cm
haven’t passed for 4-6 weeks
what are the 5 tx options for nephrolithiasis?
1. NSAIDS and opoids!!
1.5. increased fluid intake key!
2. shock wave lithotripsy (small renal caliculi)
3. precutaneous nephrolithotomy
4. rigid and flexible ureterscopy +/- stent placement
(tx of choice for maority of middle and distal urethral stones or those who failed shock wave lithrotripsy)
5. diet changes for Ca oxalate stones (decrease spinach, animal protein, Na intake)
what is the most common cause of recurrent calcium stones?
most common abnormality elevated Ca excretion, decreased serum Ca
stone passage
- explain how size and location effect the ability to pass the stone?
- what are two meds you can give to help during the passage?
size
5-10 mm less likely to pass on their own
>10 mm won’t pass on their own
location
stones in proximal ureter less likely to pass
ureterovesicular junction more likely to pass
Meds to help pass:
alpha blocker (tramsulosin)
CCB (nifedipine)
if you txing a pt with nephrolithiasis what are 3 things you want to do to help manage the pt?
when do you consider hospitalization (2)?
- most managed conservatively with pain management Nsaids and Opoids (BETTER USED TOGETHER!!)
- hydration
- strain urine
consider hospitalization:
uncontrolled pain/fever
can’t tolerate oral intake
why is it important to educate your patient on recurrence for nephrolithiasis?
⅓ will experience stone recurrence within 5 years
½ experience stone reccurence within 10 years
explain what falls under the two categories of uncomplicated UTI (2)
and
complicated UTI? (6)
uncomplicated UTI
- acute cysitits
- acute pyelonephritis
complicated UTI
- something that makes the more likely to fail treatment
- obstruction
- anatomic abnormality
urologic dysfunction
- MDR uropathogen
2. pregnant
3. elderly
4. children
5. males
6. recurrent
Complicated UTI
Pregnancy
what are 3 things its assocaited with?
do you screen?
if positive what must you do (2)?
what is one really key thing to remember about UTI and pregnant women?
associated with preterm birth, low birth weight, prenatal mortality
screen in 1st trimester with UC
admit them since dangerous with baby
always check urine culture if asymptomatic because the bacteria in the urine can cause the things under A, if + treat with abx
if they get 2+ positive tests with greater than 100,000 positive tests they they will be on suppressive abx for the remainder of the pregnancy
Complicated UTI
eldery
what are two groups of peopel that are esp susceptible?
what are three things that contribute to the first?
postmenopausal women
- bladder/uterine prolapse
- loss of lactobacilli in vaginal flor allos for E. coli to take over
- diabetes (sugar)
benign prostatic hypertrophy
complicated UTI
children
who is this more common in?
3 symptoms?
what is the DOC?
how long do you treat for, two options?
white children more common than black children
fever, hematuria, abdominal pain
DOC: 2nd-3rd line cephalosporin
7-14 days if febrile
5 days if immune competent and afebrile
complicated UTI
males
what are two risk factors?
urethra length?
unusual for men 15-50
RF: uncircumcised, anal intercourse
antibacterial material in prostatic fluid
18-20 cm urethra
who are UTIs most common in?
what is the most common route of infection?
what are most from?
what isthe pathogenisis of this and what does it RARELY come from?
30:1 ratio women to men because women have a significantly short urethra
route of infection: ascending from the urethra
UTI most commonly from uncomplifcated acute cystitis
pathogenisis:
- colonization of vaginal introitus by uropathogens from fecal flora ascend from urethra into bladder CYSTITIS
- uropathogens ascend from bladder to kidney via ureters
RARELY CAUSED BY SEEDING OF BACTERIA
what are 5 RF for UTI?
female sex
frequent sexual intercourse
diaphragm/spermicide use
delayed post-coital micturition (not urinating after intercourse)
hx of UTI
what are four bacteria that cause UTI and which is by far the most common? what percent?
e.coli most common 75-95%
proteus mirabilis
klebsiella pneumoniae
enterococcus
what are the difference in symptoms for
cystitis (6)
vs
pyelonephritis? (5)
cystitis:
- dysuria or burning while urination
- increased frequency/urgency
- suprapubic pain/discomfort
- hematuria
- voiding small amounts
- AFEBRILE
pyelonephritis
- FEBRILE
- chils
- flank pain
- costovertebral tenderness
- CBC with left shift
what 3 lab tests are important to do when diagnosiing a UTI?
what do you find on each?
1. UDIP
+ leukocyte esterase (product of baceteria)
+ nitrites (conversion of nitrates to nitrites via bacteria)
+WBC
+WBC casts (INDICATES KIDNEY ORIGIN!***)
2. hematuria
3. culture greater than 100,000
what are the DOC fo acute cystitis (4) vs pyelonephritits (2)?
what do you need to note?
acute cystitis
DOC1: TMP-SMX
DOC2: CIPRO
DOC3 if pregnant/allergic: Nitrofurantoin
***add pyridium***
acute pyelonephritis
DOC1: ciprofloxacin
DOC2: TMP-SMX
*****NOTE THE DOC FOR FOR THESE TWO ARE DIFFERENT!!!*****
what is the DOC for an inpatient with UTI/pyelonphritis?
CIPROFLOXACIN!!
others:
fluoroquinolone, amp+gentamycin, ceftriaxone
what is the most common nosocomial infection in the US? what is the tx protocol with this?
cathertized associated UTI
if asymptomatic don’t need to treat with abx
screen urine 48 hours after removing catheter
recurrent UTIs
what are the two definitions of this?
what should you consider?
what about in women with decrease in lactobacillis?
3 or more episodes per year confirmed UC OR 2 UTIs in last 6 months
consider self treatment at first sign (urine cup for UC)
vaginal estrogen in women since they have a decrease in lactobacillus
in asymptomatic bacteremia who do you treat (3) and who do you not treat (3)? *key!*
treat:
- pregnant
- before urologic procedures
- after renal transplant
DONT TREAT
- diabetics
- elderly
- patients with spinal cord injury or indwelling urethral catheter
do you tx UTI empirically while waiting for culture?
YES! then adjust abx as appropriate! :)
thelarche
pubarche
menarche
thelarche: breast development in females
pubarche: production of pubic/axillary hair
menarche: menses
polymenorrhea
consistent menstrual cycle with a length of 21 days or FEWER!!!
oliomenorrhea
consistent menstrual cycle with a length of 35 days or GREATER
dysmenorrhea
painful menstruation
how to anticholingerics decrease URGE incontinence? 3
what are the four SE to be aware of?
- increase bladder compactiy
- decreased in bladder contractions
- improve urgency sxs
SE: NO PEE, NO SEE, NO SHIT, NO SPiT
what are keagles? how often should you do them? how long should you hold them?
contraction of the pelvic floor muscles
hold 3-5 seconds
50-100 reps a day
dysfunctional uterine bleeding
what is this?
who do you most commonly find it in?
what is the MC cause?
what are the two dx tests you always do on eat pt?
dx of exclusion where abnromal bleeding without pathologic cause has been ruled out in very young or perimenopausal woman
usually an issue with the hypothalmic-pituitary-ovarian hormaone axis
MC: shortly after menarche or during perimenopause because of increased anovulatory cycles (90%) since there is unopposed estrogen it leads to irregular, unpredictable sheeding/bleeding“think: when cycle changes”
DX:
Always run:
CBC and platelents
PREGNANCY TEST
consider: all other testing needed to rule everything else out!!
how do you tx dysfunctional uterine bleeding with acute bleeding or long term bleeding?
2
4
- MC: NSAIDS
Acute:
- oral progestins
- IV estrogen for life threatening bleeding
chronic:
- cycle with low dose COP, patch, or vaginal ring
- cycle with progestin
- choice depends on sage, smoking hx, preference
- endometrial ablation
what is the most common gynecological malignancy?
endometrial cancer
endometrial cancer
who is this most common in?
what is the most common sxs of this?
dependent on what?
explain the characteristics of the two types?
5
4
what are the 4 dx methods?
MC gynecological cancer
most postmenopausal 75%, 50-60 years old
estrogen dependent cancer
mc sxs, inappropriate uterine bleeding postmenopausal
type 1:
MC type
unopposed estrogens stimulate the endometrium
well differentiated
starts as hyperplasia
curable
type 2:
endometiral atrophy
undifferentiated
clear cell and papillary serous histology
mor agressive and found at later stage
DX:
1. entometrial bx
- transvaginal US >4mm
- hysterscopy with bx
- dilation and cutterage GOLD STANDARD but not more effective, and not therapeutic
what are the tx methods for endometrial cancer? 3
what has a protective effect?
- total hysterectomy
- radiotherapy and chemo at advanced stages
- reccurence is txed with high dose progestins
OCP have protective effect?
what are 6 RF for type 1 endometrial cancer?
- obesity-fat makes weak estrogen which are unopposed after menopause and causes cellular change in uterus
- metabolic syndrome
- diabetes
- polycystic ovarian syndrome
- exogenous unopposed estrogen
- tamoxifen (breast cancer med)
explain the progession of type 1 endometrial cancer? explain the interventions throughout the process
- high weight + unoppposed estrogen+low exercise +low isofalvones leads to unhealthy endometrium
- unhealthy endometrium leads to endometrial hyperplasia (overgrowth of endometrial cells, premalignant and presents with heavy periods)
***intervene here with diet, exercise, weight loss program, hormone therapy
- if no intervention leads to endometrial hyperplasia with atypical cells
**intereven here with hormone therapy and surgery**
- if not intervention wil leads to endometrial adenocarcinoma which is CANCER!!!
explain tx options in:
- endometrial hyperplasia without atypical cells
- endometrial hyperplasia with atpical cells
- endometrial adenocarcinoma
- endometrial hyperplasia without atypical cells: diet, exercise, weight loss program, hormone therapy (progestin pO or mirena so estrogen isn’t unopposed and limits endometrial growth)
- endometrial hyperplasia with atypical cells: hormone therapy and surgery to remove effected areas
3. endometrial adenocarcinoma: HYSTERECTOMY with radiation and chemo for advanced stages
endometriosis
what is this?
where is it most commonly found?
who is it common it?
what does it cause?
classic sxs?
find on PE? 1
2 dx methods?
6 tx options?
tissue histologically that resembles endometrium found outside of the uterus, MC on ovary and pelvis, that responds to cycical hormonal changes, at less than 35 years old who is nullparous (not given birth to child)
mc cause of infertility 25-35%
classic triad:
- cyclic prementrual pain, pelvic area
- dysmennorhea (including spotting)
- dyspareunia (with deep thrust)
PE:
tender nodularity of the cul de sac and uterine ligs
DX:
- US
- laproscopy
Tx: (based on sxs and location, child bearing desire)
- NSAIDS
- OCP-relieve sxs
- progestins- reduce flow, ovulation and cause less bleeding/discmfort
- danazol
- GnRH-block release of pituiatry hormoens governing menses
- surgery-last resort if fertiliy is to be maintained
leiomyoma aka fibroids
what is this?
who is it MC in? 2
what is it dependent on so who is more likely to get this?
2 sxs?
pe finding?
dx? 3
benign uterus smooth muscle tumor, MC in african americans and those older than 40
small, to large, singe, multiple
estrogen dependent and seen more comonly in those who have endometrial hyperplasia, anovulatory statees, and estrogen producing ovarian tumors
SXS:
bleeding is MC sxs
mennorrhagia
PE:
firm, enlarged, irregular uterine mass
DX:
Pelvic US
D&C
laproscopy
how do you tx leomyoma or uterine fibroids? 6
depends on the age, parity, reproductive plans, general health, size and location
1. observation-MC
- GnRH agonist-shrink fibroid 6 months only
- OCP/IUD progestin-inhibit estorgen
- myomyectomy-high risk of reccurence so done close to when she wants to become pregnant
- hysterectomy *definitive*
- uterine fibroid embolization (UFE)
explain the 5 different types of leomyomas/fibroids and their location?
`1. pedunculated: bubble off uterus with stock
- intracavity: within uterus
- intramural: within the uterine muscle
- submucous: directly under the endometrium, causes uterine bleeding
- subserous: directly under the serous lining, outside of the muscle
what are two risks that are increased if a woman has leomyomas or fibroids?
- endometrial cancer 4x
- spontaneous abortion
pelvic organ prolapse
what is this?
what are the 2 RF?
what are 2 key sxs? 3
PE? 1
5 tx options? 2 key
one organ protruding into another where it isn’t supposed to be
RF:
weakness of pelivic floor muscles
MC cause: childbirth
SXS
pelvic fullness, heaviness, and “falling out” sensation or “sitting on a ball”
low back pain esp with prolonged standing that improves after laying down
urinary frequency urgengy and stress
PE:
bulging mass est with increased intrabdominal pressure ie valsalva
Tx:
- DO NOTHING IS ASYMPTOMATIC!!!
- pessaries
- keagles
- estrogen (improve atrophy)
- surgery
pelvic organ prolapse:
uterine prolapse
what is this?
what are the 3 types?
uterine herniation into the vagina
Types:
anterior wall desent: protrustion of the urethra into vaginal canal
posterior wall descent: protrusion of the rectum into the vaginal canal
central prolapse: protrusion of the uterus into the vaginal canal
pelvic organ prolapse:
cystocele
posterior bladder herniating into anterior vagina
pelvic organ prolapse:
rectocele
distal sigmoid colon (rectum) into the posterior distal vagina
what are the 5 RF or causes of pelvic organ prolapse?
- age MC after menopause, risk increases to 50% post menopause
- parity-vaginal delivery
- obesity-increased intrabdominal pressure
- chronic cough
- chronic constipation
what is the grading for pelvic organ prolapse?
grade 1: dsecent into the upper 2/3 of the vagina
grade 2: cervix approaches the introitus (vaginal canal)
grade 3: outside introitus (seen outside body)
grade 4: entire uterus outside of the vagina-complete prolapse
Cervical Cancer
what is it?
what 4 things most commonly cause it?
IT IS A STI!!!!
HPV in 99.7% of cases
HPV: 16, 18, 31, and 33
Cervical cancer
what are two important stats on this?
where does this likely occur?
what are the two most common histological types?
3rd most common GYN cancer in US and #2 of ALL CANCERS in women worldwide
usually occurs at the transformation zone (at SJC junction between squamous epithelium and glandular epitelium)
squamous cell 69%
adenocarcinoma 25%
explain the progesson of cervical cancer and why this is considered a cancer that effects 40-50s and why we screen in younger women?
cervical dysplasia is a precursor for cervical cancer
Cervical intraepithelial neoplasia CIN is the preinvasive phases of cervical cancer (it isn’t cancer yet!)
carcinoma in situ CIS is the first cell change to cancer
Ages:
20s: common occurance of CIN
25-35: CIS becomes more common in addition to continuation of CIN
40-50: Cervical cancer
explain the ranking of cervical intraepithelial neoplasia (CIN)?
CIN1: mild dysplasia
CIN2: modterate dysplasia
CIN3: severe dysplasia
**1/3 of patients will progress to carcinoma**
CIS: carcinoma in situ
how do you prevent cervical cancer?
gardisil vaccine
protects: 6, 11, 16, 18
reccomended ages for bots and girls 11-26 years old
why was the pap smear considered a epidemology succes?
decreased the insicidence and mortality from cervical cancer 75% in the last 50 years in developed countries, 95% according to hoffmans lecture?
what symptom and PE findings are found with cervical cancer?
what do you use to dx?
what are the tx options?
3
SXS:
early cervical CA is asymptomatic
irregular or heavy vaginal bleeding
post coital bleeding and spotting MC sxs
PE: possible lesions that are raised and friable
DX: colpscopy with bx
Tx:
if early stage <4 mm and confined to cervix can be cured via:
- radical hysterectomy
- fertility-sparing surgery
- radiation and chemo
if metastic of reccurent, media survival is less than 2 years
explain the process of performing a colposcopy? what is it used for? what are 2 management tecnniques?
used to follow up abnormal pap results
magnifies cervix
cervix stainged with acetic acid (vinegar) or iodine to identify the areas that need to be bxed
tx/management options
- loop-electrosurgical excision procedure (LEEP)
- ablation of T-zone with cryrotherapy or laser
what are you intervention options based on the possible cervical bx results?
- mild lesions may resolve spontaneously
- preinvasive neoplasia can be txed with electrocautery, cryocautery, laser surgery, conization, large loop excesion of transitional zone, or LEEP procedure (Green book)
explain HPV 16 and 18 and what they are likely to cause?
responsible for 70% of cervical cancers
16: higher rates of squamous cell cancers CIN3
18:** higher rates of **adenocarcinomas
what percent of woman who get cervical cancer never got a pap?!
50%
what are the screening guidelines for a pap smear?
- start at age 21 until 65 (don’t check if under 21 and sexually active)
- screen every 3 years from 21-29
- pap + HPV “co-test” every 5 years if between 30-65
**notice you don’t screen for the actualy HPV virus if you are under 30
incompetent cervix
or
cervical insufficency
what is this?
what are 4 RF?
what are 3 sxs?
2 tx options?
premature cervical dilation established in the 2nd trimester
RFs:
- previous cervical trauma/procedure
- uterus defects
- DES exposure in utero
- multiple gestations
SXS:
- vaginal bleeding
- vagininal discharge esp in 2nd trimester
- painless dilation and effacement of cervix
TX:
1. bedrest
2. cerclage (suturing of cervical OS)
Vaginal and vulvar neoplasms
what are these associated with?
how common are each?
who do you find them in?
in the second…what is the MC precention?
what do they look like?
premaligment and malignant lesions commonly associated with HPV
vaginal intraepithelial neoplasia (VAIN)**/**vaginal cancer
RARE less than 1% of all GYN cancers
women over 50
MC presentation is postmenopausal blleding or bloody discharge
vulvar intraepithelial neoplasia (VIN)/vulvar cancer
3-5% of all GYN cancers
MC are squamous cell carcinoma in postmenopausal woment
younger women with warty lesions assocaited with HPV
older women less associated with HPV
puritis MC precention or asymptomatic
red/white ulcerative crusty lesions
vaginal and vulvar cancers
how do you dx?
3 tx options?
DX:
colopscope
Tx:
excision
laser
tropical antineoplastic agents
- 5-FU
- imiuimod
lichen sclerosis
what is this?
2 sxs?
what are the characterisitcs of acute and chronic lichen sclerosis?
3
2
what does chronic produce a higher risk of?
tx goal? tx?
MC vulvar dermatological disorder
benign chronic inflammatory process
SXS
- pain
- dysuria from loss of elasticity
ACUTE
red/purple lesions on non-hair-bearing ares in the perineum and perianal area in a hourglass pattern
- erythema and edema
- white plaques (keratosis)
- intense puritis
Chronic
skin becomes thin, white, and shiny
can lead to loss of genital landmarks
- labia fusion
- introital stensosi
Tx:
STOP SCRATCH ITCH CYCLE
-STEROIDS
what does lichen sclerosis put you at increase risk for?
squamous cell carcinoma
bartholin’s cyst
what is this?
what are the 4 sxs?
dx?
3 tx methods?
obstruction of the duct of bartholins gland causing retention of secretions and cystic dilation that can cause infection
SXS
non infected: minimal
infected:
pain, tenderness, erythema, dyspareunia with fluctulant mass
DX:
culture/cbc
Tx:
none if asymptomatic
drain with ward catheter or marsupulize
excisions if recurrent
bartholins glands
what are they?
what are their functions?
two glands located slightly posterior to the left an right of the opening of the vagina
function:
secrete mucous to lubricate the vaginal opening 1-2 drops when sexually aroused
Amenorrhea
what is this?
what are the two types?
what are they qualifications for both?
what is the most common cause of the last?
what are 6 other causes?
the absense of a menses
primary: never had menses, younger girls
-absense of menstruation before age 16
secondary: had menses and stopped for 3 months if cycles are normal, or 6 months if the cycles are irregular
most common cause is pregnany!!
others:
- drug use
- stress
- weight gain
- excessive exercise
- Asherman’s syndrome-acquired endometiral scarring
- polycystic ovary syndrome
Ammenorhea
what are two tests you want to run for this?
what are two tx options?
DX:
- PREGNANCY TEST EVERYTIME!!!
- progesterone challange
idirectly determines if the ovary produces estrogen
if endometrium is primed with estrogen (functioning ovaries) progestin will produce menses
expect withdrawal bleeding within several days of completing progestin course
Tx:
- OC
- cyclic progesterone for 5-12 days a month for smokers for over 35 year olds
dysmenorrhea
what is this?
what are the two types and their characteristics?
what age group are they common in?
painful menstruation
primary
not due to pelvic pathology due to excess of prostaglandins and leukotrienes** leading to **painful uterine contractions, N/V/D
starts 1-2 years after the onset of menarche in teenagers
secondary
due to pelvic pathology so a identifiable condition
25 years and older
endometriosis, adenomyosis, uterine fibroids, PID, IUD
dysmenorrhea
what are the sxs associated with primary and secondary dysmennohrea?
what are the tx options for both?
sxs
primary:
- cramping, bloating, and lower abdominal pain that radiates to the back or thighs
- begins before or during menses for 1-3 days
secondary:
the above PLUS
- bloating
- mennorrhagia/dyspareunia
tx:
primary:
NSAIDS
heat, exercise, OCP
secondary:
tx underlying condition
premenstrual sydrome
what is this?
when does it occur?
what must be present?
what percentage of women get this?
what two tests shoudl you do?
what are the 5 tx options?
cluster of physical, behavioral, mood changes with cyclical occurence during luteal phase of the menstrual cycle
occurs 1-2 weeks prior to mentstraion and ends 1-2 days after the onset of sxs
a symptom free period during the follicular phase, day 1 of menses must exist
75% of women have some symtpms of this
5% have severe sxs and distress that limit their ability to participate in lfe basically
DX:
thryoid to rule out thyroid issues
CBC to rule out anemia
Tx:
1. limit caffine, alcohol, sodium
2. frequent high-complex carb meals
3. stress management/exercise
4. SSRIs 14 days prior to the onset of menses
5. NSAIDS
menopause
what wualifications does this have?
what age does this occur around?
what do the symptoms come from?
4 sxs?
3
3
cessation of menses after 1 year loss of ovarian activity at approximately 51
SXS:
vaso motor sxs from decreased estrogen production
1. HOT FLASHES upper body, face, chest, and neck
- interfere with sleep
- 75% have them
- last 6 months -2 years depends on person
2. atrophic vaginitis with discharge and itching and loss of elasticity
-can lead to dyspareunia and sexual dysfunction making a low quality of life, self-esteem, and sexual intimacy
3. sleep distrubances
4. new onset depression
menopause
what are the 3 tx options?
- systemic hormone therapy most effective estrogen or progesterone with the lowest effective dose and shortest duration but limited to 5 years or less of use
- SSRIs 2nd
- SNRIs
what must you consider when txing women for menopause with hormone replacement therapy?
use progesterone and estrogen as hormone therapy for this
must consider if woman has uterus or not BEFORE giving hormone therapy
- if no uterus: can use esterogen alone
this is the most effective tx, however, it increases the risk for endometrial cancer so you ONLY use it patients WITHOUT a uterus
- if uterus: must use estrogen AND progesterone
NO icnreased risk for endometrial cancer so can be used in patients with a uterus slightly increases risk for breast cancer so must keep this in mind
how do you dx menopause in woman? what if you wanted to check labs? what are they at increased risk for?
typically a clincial dx
in labs you would use FSH to dx because this would be high as well as LH while the estrogen levels are still low
they are at increased risk for osteoporosis so may want to consider putting them on medicalion to prevent this
giving someone estrogen increases their risk for?
BREAST CANCER
giving someone unopposed estrogen increases their risk for what if they have a uterus?
endometrial cancer
estrogen has protective effects over what?
OSTEOPOROSIS
infertility
what is this defined as for the different age groups?
what are the 3 most common cuases?
what are 4 RF?
failure to conceive past 1 year of unprotected regular intercourse** **in women less than 35 and after 6 months in women older than 35
30% male, 30% female, 25% unknown
RF:
- cigarette smoking
- radiation
- chemo
- autoimmune dxs
what is the oocyte aging process?
numbers?
degeneration accelerates quickly at?
when do you see the largest population of people seeking fertility help?
OOCYTE aging
1. decrease in both the quality and quantity of oocytes
- 1-2 million follciles at birht to 300,000 at the onset of puberty
- loss acceralates quicky at 30s
35-39 is when you see the biggest population of couples seeking fertility help!!
female infertility
what are 6 causes of female infertility and what are the two most common causes?
- ovulatory disease MC 25%
PCOS, eating disorders, CUshings, CAH, Turners, thyroid disease
- endometriosis 15%
damage or lining changes prevent ovulation fertiliation and implantation
- pelvic adhesions
- tubal blockage
- uterine fiboirds
- congenital defects
male infertility
what are the 3 branches of male infertility causes?
what is the MC cause?
4
3
1
- testicular disease 30-40% MC
Klinefelders syndrome
varicocele
Y chromosome deletions
STIS
- disorders of sperm transport 10-20%
epididylmal dysfunction
vas deferens dysfunction
ejaculatory dysfunctions
- hypothalamic pituitary disease (secondary hypogonadism) 1-2%
what are 7 test you would want to check in a woman who is infertil?
- FSH-ovarian function at day three
- TSH-thyroid function
- menstrual hx
- LH surge prior to ovulation or luteal progesterone
- prolactin
- pelvic US
- hysterosalpingogram (HSG)
what four testing methods would you want to use in a male who is infertil?
what does the first asses for? 5 things
exaplin the collection requirements?
- semen analysis
volume and pH
asses sperm:
motility, concentration, and morphology
leukocyte count
immature germ cells
collect 2-7 days after abstinence, need at LEAST 2 samples collected 1-2 weeks apart
- decrease alcohol, marijuana, tobacco use
- endocrine levels
- genetic testing
who do you asscess for infertiliy in these groups:
- after 12 months of unprotectedand frequent sex
- after 6 months of unprotected and frequent sex
- upon presentaiton
- under 35 y/o after 12 months
- 35-40 y/o after 6 months
- upon presentation
- over 40
- amenorrhea
- hx of chemo, radiation, end stage endometriosis
- uterine or tubal dx
- male with hx of groin, testicular surgery, chem, or radiation
what are the 5 tx objections for someone with infertility?
3 under female
3 under male
- smoking cessation
- decreased caffine, alcohol use
- appropriate timing of sex around ovulation time using predictor kit
-
therapeutic interventions
- clomid ovulation stimulator
- interuterine insemination (IUI)
- in vitro fertilization (IVF) - male tx
hypogonadism from hyperprolactin: bromocriptine to lower prolacting
- other hypogonadism: HcG injections
- sperm disorders: retrograde ejaculation
if someone has unexplained infertility what should be the first and second step to try to tx it?
- climpiphene + intrauterine insemination since low cost and low SE
- gonadotropin injections and interuterine insemination
adenomyosis
what is this
who does it occur in
what are 3 sxs
what might you find one PE?
3 dx tactics
4 tx options
uterine thickening that occurs when entometrial tissue invades the myometrium, and can cause a mass in the uterus called a adenomyoma
unknown cause
MC: women older than 30 who have had children, increases with age!
SXS:
tender and “boggg” uterus
mennorrhagia (heavy menses)
dysmenorrhea
PE
enlarged uterus
uterine mass
DX:
US
endometrial sample
MRI
Tx:
- nothing
- progestin containing IUD (supress bleeding and allows mass to shrink)
- OC
- surgery last chance
premenstrual dysphoric disorder
what is this?
what does it do?
what must you have?
and the many sxs?
basically PMS on steroids that disrupts daily living
must have 5 or more of these symptoms and occur the week before the onset of menses and start to improve within a few days after the onset of menses and not during other times
- marked affective lability (mood swings, sensitivity)
- marked irritability or anger or increased interpersonal conflicts
- marked depressed mood, feelings of helplessness, self-depreciating thoughts
- marked anxiety, tension, feeling of being on edge
- decreased interest in usual activities
- subjective sense of difficulty in concentration
- lethargy, easily fatigued, marked lack of energy
- marked change in appetite, overeating, or specific food cravings
- hypersomnia or insomnia
vaginitis-candida
what percent of women get this?
what are the 3 causes?
3 sxs?
2 dx?
2 tx options?
75% of women have it at least once
candida albicans MC and causes 90% of cases
also candida glabrata and tropicalis
SXS:
cheesy white discharge
intense itching
inflammed vagina and vulva
DX:
clinical
wet prep with KOH
Tx:
imadazoles oral or topical
recurrent: likely glabrata or tropicalis
fluconazole for 2 weeks
do you tx the sexual partner of someone who has candidal vaginitis?
only if they are asymptomatic!
atrophic vaginitis
what is this the combination of?
when are 3 times this is more likely to happen?
4 sxs?
tx?
caused by the combination of
low estrogen
- prepubertal
- post menopausal
- after childbirth esp if nursing
and
thinned vaginal epithelium
SXS
dryness, spotting, seroanginious discharge, dyspareunia
Tx:
intravaginal estrogen
women who are exposed to diethylstilbestrol (DES) are at increased risk for….
clear cell adenocarcinoma of the vagina
vulvodynia
what is this?
what are the 2 types?
sxs?
8 tx options?
vulvar pain in the absence of physical findings
1. PROVOKED
20-30 year olds
comes after something like childbirth or infecion
vestibular erythema
tendernress
introital pain
2. UNPROVOKED
over age 40-60
larger area of pain
cause unknown
SXS
burning, irritation, hyperalgesia
Tx
- pelvic floor pT
- lidocaine
- tea tree
- topical estrogen
- tricyclic antidepressant
- gabapentin
- vulvar vesticuloectomy
- chronic pain referral
squamocolumnar junction (SCJ)
what is this and what type of cells are involed?
what happens as you age?
what happens here?
how much does it move?
where the inner lining of columnar cells** meets the **exterior sruface of squamous cells
“eversion of the columnar epithelium onto the ectocervix”
however this moves inward over time which is why you cant see it
transformation zone:
- where metaplasia and hyerplasia occur
- neoplastic changes occur here
- can be visualized in younger people (pic) but not in older peopel ebcause it moves into the cervical canal approximately 3cm from original location
nabothian cyst
yellowish translucent pear-like shaped cyst on the ecto cervix
cervical polyps
what are characteristic of these? 6
who are they common in?
how do you dx?
small, pedunculated neoplasms, red, FRIABLE that originate from the endocervix and protrude 2-3 cm
very common esp if older than 20, most are BENIGN
DX:
remove by grasping with forceps and twisting to send to pathology to r/o malignant changes
cervical stenosis
wat is this?
what are 4 causes of this?
narrowing of the endocervical canal, usually at the OS, with partial to completely occlusion of the OS
causes:
- congenital
- hypoestrogenic
- neoplastic
- post surgical
what percent of pregnancies are unintended?
49%
what are 6 things you need to ask a patient before prescribing BC?
- blood clots DVT/PE
- pregnancy hx (rule out w/test)
- clotting disorders (factor V lieden)
- medications/allergies
- smoking status
- weight/BP
what are two things you must rule out before prescribing BC?
COC: BP (no HTN)
IUD: pelvic exam, rule out STIs
long acting reversible contraception (LARC)
what is the pregnancy rate?
who can the be used in?
2 worse SE?
what are the 4 options for this?
MOST EFFECTIVE, pregnany rate less than 1%
can be used in all women including adolescence
bad things: longer bleeding and worse cramps
OPTIONS:
1. Nexplanon implant
2. paraguard COPPER IUD
3. Levonorgestrel release IUD
-mirena
-liletta
-Skyla
4.methdroxyprogesterone acetate depo-provera shot
LARCs:
Nexplanon-estronogestrel implant
what hormone is used?
how long?
menses effect?
wouldn’t want to use in somoene….
Hormone: progestin
duration: 3 years
menses: lighter, irregular with unscheduled bleeding
Don’t use: in someone who poor tolerance to amennorhea or unscheduled bleeding
LARC:
paraguard IUD
hormones?
duration?
menses effect?
3 risks?
6 epeopl you don’t use it in?
hormone: NONE!!! COPPER ONLY!!
duration: 10 years
menses: may get heavier with more cramping and unscheduled bleeding
risks: uterine perforation, expulsion, infection
don’t use:
- heavy ir painful menses
- iron deficiency
- anemia
- uterine abnormality
- copper allergy
- wilsons disase
foreign body rxn and chemical changes may be toxic to sperm and ova
LARC:
levnorgestril release IUD
3 options?
hormone?
duration?
menses effect?
poor choice for 2?
3 risks?
mirena
liletta
skyla
hormone: progestin
duration: 3-5 years depending on type
menses: lighter and irregular with unscheduled bleeding
risks: uterine perforation, expulsion, infection
poor choice: lower tolerance to amennorhea or unscheduled bleeding
LARC:
medroxyprogesterone acetate
depo-provera
pregnancy rate?
hormone?
administration timing?
menses effect?
2 risks?
poor choice for?
pregnancy rate 6% first year of use
hormone: progestin
injection: every 12 weeks (3 months)
menses: lighter and irregular with unscheduled bleeding
risks: weight gain and mood swings
poor choice: for quick return of fertility
combination hormonal contraception (pill/patch/ring)
pregnancy rate:
hormone:
3 options and duration
menses effect
pregnancy rate: 9%
hormone: progestin and estrogen
pill: many combinations- 28 day, 21 day, extended cycle
ortho evra patch-
Nuvaring-_monthly_
menses: lightr, regular predictable withdrawal bleeding with cyclic use
combined contraceptive options
pill, patch, ring
11 contraindications you should know!
RISKS/Contras:
- breast cancer
- estrogen/progestin dependent neoplasms
- hepatic tumors
- stroke
- DM with vascular
- DVT/PE
- hypercoagabilities (factor V)
- migraines with aura
- HTN uncontrolled
- rythmn dxs lik afib
- women older than 35 smoke
potential noncontraceptive benefits of cyclic estrogen-progestin contraceptive? 7
- reduction in dysmennorhea with more regular cycles
- reduce risk of etopic pregnancy
- reduce PMS PMDD
- decrease ovarian cancer
- reduced endometrial cancer
- reduction in acne
- reduced hirsutism
what are two increased risks when taking BC that contains estrogen?
- increase risk of breast cancer
- increase vascular thrombolytic event from increased lipids (DVT/PE, AMI/CAD)
what are the 3 processes for steralization and what does each process entail?
- Essure
hyteroscopic steralization-metal coil inserted into the distal portion of each fallopian tube office based procedure under anastesia
- bilateral tubal ligation
laparoscoptic vs mini-lapro
samoe day surgery
- vasectomy
non-scapel vasectomy-puncture is made through the scrtom skin overlying the vase defference and widened only enough to externalize the vas deference for transection
officed based under local anastesia
need 20 ejaculates to get the left over sperm out
barrier methods including male condoms, effective?
greater for STIs, not great for pregnacy 18% failure rate
how long can a pulse of GnRH last?
anywhere from 15 mins to 2 hours
explain how hormonal contraception works? 3
1. inhibits secretion of pituitary gonadotropins via NEGATIVE feedback mechanism which prevent follicular follicle development and ovulation
2. alters endometirum (thinning) which may effect implantation by producing unfavorable environment for fertilization
3. thickens cerivcal mucous which inhibits sperm passage/penetration
what are the two most common emergency contraception options?
- levonorgestrel OTC (so convient) “plan B” 50-94% efficacy
- ulipristal Rx “Ella” 98-99% effective **MOST EFFECTIVE oral**
- paraguard *MOST EFFECTIVE METHOD*
how many menstrual cyles does a woman experience on average in her lifetime
about 400
explain the link between estrogen and breast cancer?
nullparity (not having children) increases the risk for breast cancer because it increases the number of menses the woman has thus increasing the amount of unopposed estrogen she is exposed to
this stimulation of cell proliferation during every cycle increases the risk for development of breast cancer
those who have early menarch and late menopause are also at increased risk because it increases the number of menses they have and ultimately exposes them to more estrogen
first pregnancy appears to have a protective effect
COOL FACT: THIS IS WHY NUNS HAVE A HIGH RISK FOR BREAST CANCER!!!
Why is it important that GnRH is released in pulses rather than continuously?
Pulsatile release: maintains normal FSH, LH levels in the blood
as GnRH is released it binds to gonadotrophs and causes released of STORED LH and FSH
**allowing a period of rest between pulses allows the gonadotroph to increase stores aka priiming effect**
continuous release: results in a REDUCTION of the pituitary contens of FSH and LH and their release (since trying to replenish stores)
clinical implications
GnRH agonists and antagonists: down regulate LH and FSH release since it continiously sitmulates receptors and doesn’t allow for the gonadotrophs to replemsih stores
these can be used in certain cancers to lmit the amount of estrogen/progesterone they are exposed to since this is the ultimate product of this process.
**may cause an intial flare in sxs and then down regulate**
- breast cancer
- endometriosis
- prostatic cancer
what are seroids made from? explain their carbon and conversion properities?
steroids are made from cholesterol which comes from acetate
progesterones: 21 carbons
androgens: 19 carbons
estrogens: 18 carbons
converstion of one steroid to another can be accomplished by enzymes that are a part of the cells biosynthetic package where carbons can be taken away but NOT added
aka a progesterone can become an estrogen but an estrogen can’t become a progesterone
what are most steroids produced from?
most likely acetate with the intermediate as cholesterol, however, direct synethesis also occurs with cholesterol that is produced by the liver or supplied by the diet
what is the first step of ALL steroid synthesis? what is this catalyzed by? explain the feedback between this and HMG coA reductase?
FRIST STEP: converstion of cholesterol to pregnenolone “MOTHER OF ALL STEROIDS” since all steroids stem rom this and process which occurs in the mitochondria of ther steroid producinc cell
this process is cataliyzed by mitochondrial cytochrome P450 side chain cleaving also referred to as desmolase 20-22
cholesterol is a negative feedback regulator of HMG CoA reductase….so when cholesterol is high this enzyme decreases, when cholesterol is low this enzyme increases
***THINK ABOUT IT: this is why HMG CoA reductase inhibits work for someone with high cholesterol, it prevents further synthesis!***
explain the solubility of steroids? what consequences does this have? 3 options? explain the difference in affinities?
structually similar to cholesterol since that is what they are derived from so they are
highly fat soluble and poorly water soluable….this means you find them bound to plasma proteins in the blood. MC albumin, sex steroid hormone, and cortisol binding globulin
albumin: low affinity for bound steroids, weak bond
sex hormone binding globulin (SHBG): high affinity for androgens (testosterone) and estrogens but low affinity for progestens and cortisol, strong bond
explain what is meant by bioavaliable steroid?
when you ask for a the lab to quantify the serum steroids it is a combination of BOTH ‘free” unbound steroids and bound steroids (how most are)
bioavaliable steroid referrs to both the bound and unbound steroid present
what is the free angrogen index?
meaures the amoutn of bioavaliable testosterone in a person
this can help to explain a pt who presents with hirsuitism or features suggesting androgen excess
explain the relationship between sex binding hormone globulin and testosterone levels between males and females?
the majority of steroids are bound with proteins in the blood. many are bound with albumin, but many are bound with sex hormone binding globulin (SHBG)
when bound with SHBG the steroid becomes inactivated.
In men, more percent of testosterone is bound to ALBUMIN and therefore dissociates quickly, where in women is bound to SHBG and therefore is inactivated!
This explains the higher andronization of males than females because the testosterone is more bioavaliable
do changes is steroid levels greatly effect the serume concentrations/steroid effects?
not usually…..the carrier proteins like abumin and sex hormon binding globulin are always in excess of steroids, so if there are massive increases they can accound for this and it will have little effect on the body
the problem arises when there isn’t enough binding proteins like ablumin or SHBG where the slight changes in hormones show their effects more readily and is seen in conditions like liver diseases
are sex steroids like progesterone, testosterone, and estrogen kept at high or low plasma levels? why?
very low (much lower than cholesterol) with binding proteins like albumin and sex hormone binding globulins
want to keep these low because they are like cholesterol and are lipid soluble, this means that they can readily enter the cell
if these were present in high concentrations in the plamsa, they could readily enter the cell and disrupt the membrane integrity!
this is why even small levels of plasma steroids are present in the bound protein form
where are steroid hormone receptors found? and what are they bound to? what happens once they are stimulated?
found intracellular in both the nucleus and the cytoplasm often bound to heat shock proteins, that when stimulated by a steroid disocciate and bind to non steroid ligands like Thyroid hormones or vitamins
once stimulated: they undergo conformational change that allows them to recognize hormone-resonse elements (HREs) in the DNA which then allows for protein transcription/production
where are most sex steroids produced? exception? role of target organs? what enzyme?
most sex steroid hormones (progesterone, estrogen, and testosterone)** are made in the **gonads** with the exception of a **pregnant female
however it has been made clear the target organs have the ability to** **participate in INTERCONVERSION of one steroid to another thus they can take a ciculating hormone and transform it enzymatically into another steroid to use LOCALLY via its biosynthetic package of enzymes
EX:
5alpha-reductase converts testosterone to 5alpha-dihydrotestosterone “DHT” which is stronger!
what is the clinical correlation between 5alpha-reducatase and DHT levels? what percent of tesosterone is involved in this?
5alpha reducatse converts testosterone to DHT which is a stronger vesion of testosterone
5-8 % of total testosterone is converted to this
5alpha-reductase inhibitors, AKA FINASTRIDE, PREVENT the conversion of testosterone to DHT which can support the development of benign prostatic hypertrophy so reducing this enzyme in men helps to shrink enlarged prostates, can also help with baldness since DHT also contributes to this
hypothalamo-pituitary-gonadal axis
what is the pathway for production of steroids? how are they released?
HYPOTHALAMUS: RELEASES GnRH
TRAVELS VIA HYPOPHYSEAL PORTAL VEINS TO
ANTERIOR PITUITARY RELEASE FSH AND LH
TRAVELS VIA BLOOD TO
THECAL/GRANULOSA CELLS RELEASE ESTROGEN, PROGESTERONE, TESTOSTERONE
keep in mind GnRH and FSH/LH released in CHICORDIAL PULSES!!
hypothalmic gonadotrophic releasing hormone
what is this?
where is it encoded?
why is it difficult to measure?
neurohormone
encoded on chromosome 8 on single gene
serum levels: difficult to obtain since its release is confined to the hypophyseal portal blood supply and it has a short halflife 2-4 mins
FSH/LH
what is anothe rname for these?
what are they made of?
which is cleared fast which is cleared slow?
“gonadotrophins” since they effect gonad steroid synthesis in BOTH sexes
both contain alpha (identical) and beta subunits (different)
gylcosylated with sugar
FSH is cleared more slowly since it has more carbohydrates and this explains why when looking at infertility you check this because it provides more of a picture while LH is cleared fast and only provides a snapshot
inhibins
activins
effect FSH release from anterior pituitary
inhibins: allows only one follicle to be selected as graafian
activin: allows for developement
why is it important to consider CNS injury/damage in infertility?
GnRH is considered the most important final common mediator of ovulation
because the hypothalmus is the first step in the
hypothalamo-pituitary-gonadal axis process to release GnRH
OVULATION is needed for PREGNANCY so must have these pieces working if you want to get pregnant!!
CNS can lead to infetility issues
follicular phase
what does this refer to?
when does it occur?
2 key points?
OVARY from first day of menses to ovulation ~10-16 days
Key points:
- new antra follicles are recruited to proliferate
- one of these will be selected as the graafian follicle
proliferative phase
where does this occur?
when does this occur?
what are the 2 main things that occur?
UTERUS from the first day of menses to ovulation
- the uterus is under the influence of increase estrogen and the stratum functionalis of the endometrium proliferates from 1-2 mm to 8-10 mm in thickness
- increase in estrogen promotes the formation of progesterone receptors in the uterus so it can respond to progesterone in the post ovulatory phase of the cycle
ovulation
what is this marked by?
what causes this?
where does fertilization occur?
the Graafian follicle during the follicular phases ruptures in response to midcycle FSH/LH surge causing the occyte to be expelled from the follicle into the fallopiian tube
viable for ~24 hours where if sperm enter the oocyte can be fertilized at the
ampullary-isthmus junction
luteal phase
when/where does this occur?
what are the 2 things that occur?
OVARY after ovulation until onset of next menses (assuming pregnancy doesn’t occur
- corpus luteum (formerly graafian follicle) is functional unit of the luteal phase and produces increased levels of progesterone
- occurs 13-15 post ovulation
secretory phase
where does this occur?
when?
what is it marked by? goal?
if no implantation?
UTERUS after ovulation until next menses
- high levels of prosterone secreted from corpus luteum have a “quieting’ effect on the unterine endometrium and facilitate
- secretions from the uterine endometrial glands to make condusive for implantation of a blastocyst
- if no implantation: the corpus luteum dies and the endometrial tissue looses its blood supply since loss of progesterone production and causes necrosis of linging and sloughing!! MENSES and the begining of a new cycle
embryonic ovary
what is the final goal of this step?
explain the 4 phases of this developement?
- oogonia undergo MITOSIS for 3-4 months
- Enter meiosis I and are called OOCYTES
- they become arrested in PROPHASE of the first meiotic division
- start to be surrounded with PRE-granulosa cells and is termed
primordial follicle
folliculogensis
explain folliculogensis up until the formation of the graafian follicle?
explain gonadotropin dependent and indepent phases?
5 steps
- pulsatile LH and FSH released at puberty“awaken” the primordial follicles
- primoridial follicles become primary follicles with zona pellucida that serves as attachment for the granulosa cells
- primary follicles become secondary occytes or “pre-antral follicles” where the granulosa cells increase in size and the thecal layer forms
***up until this point the the development has occured INDEPENDENT OF GONADOTROPINS***
- LH and FSH increase in response to decreasing estrogen and progesterone from the previous cycle stimulating the pre-antral follicle to tern into a tertiary follicle
- one of these is selected as the graafian follicle
summary of the follicular phase
explain all the steps of this
Increasing FSH and LH cause an increase of estradiol 17B which initially has a NEGATIVE FEEDBACK of FSH and LH causing the storage of FSH and LH via decreased GnRH release
as the follicle develops from early follicular phase to late follicular phase, the LH receptors that were originally present on only the thecal cells become present on the granulosa cells where the FSH receptors are. during this time the number of granulosa cells size and number are increasing and thecal membrane formation
the increase in LH binding to these receptors (as stated above) causes the production of andosteridione, which is convered to estrogen via aromatase enzyme
this process increases the NET ESTROGEN to an extent that it causes POSTIVIE FEEDBACK on GnRH in the hypothalamus and rlease of FHS and LH and a LH SURGE that is a PARADOX (FSH doesn’t surge because of the increase of inhibin A levels rise as estogen rise)
LUTEAL surge causes the estrusion of the oocyte from the follicle and completion of meiosis I.
OVULATION!
explain the postive and negative feedback cycles that are seen in the menstrual cycle?
low levels of estradiol 17 B feedback NEGATIVELY on FSH and LH release at both the level of both the pituitary and the hypothalamus in the early follicular phase and in the luteal phase
HOWEVER, in the late follicular phase very high plasma levels of estradiol 17 B promote a POSITIVE feedback on both the pituitary and hypothalamus which is necessary to facilitate the midcycle surge of FSH/LH just prior to ovulation
explain how hormonal contraception methods play into the negative and postivie feedback mechanisms of the menstrual cycle?
if you use low levels of estrogen “low estrogen pill” it is inhibitory on FSH and LH and so you never get the LH surge which prompts ovulation! this means the ooccyte is never released into the fallopian tube
also prevents the lining of the endometrium from proliferating since this also suppresses progesterone
given the menstrual cycle–what could you do if the patient was having a hard time getting pregnant from natually low levels of estrogen?
the low levels inhibit FSH and LH release with halts the whole process
give pt clophene citrate** that is a **estrogen antagonist** that increases these levels by **knocking out the low estrogen levels
this plays of the feeback mechanisms
explains what happens to the LH and FSH receptors during the mentrual cycle?
early to mid follicularp phase:
1. LH receptors are only found on the thecal cells (outer layer) of the dominant follicle
- FSH only found on granulosa cells
mid to late follilcular phase:
- LH receptos begin to appear along with FSH receptors on the granulosa cells of the selected follicle
******MAKES IT MORE RESPONSICE TO THE LH SURGE WHICH STIMULATES OVULATION AND THE DEVELOPMENT OF THE CORPUS LUTEUM POST OVULATION****
luteal phase summary
describe all the aspects of this
the increase from the LH surge “lutinizes” (give the ability to make progesterone to the corpus luteum through stimulation of the LH receptors on the thecal and granulosa cells
causes massive** **progesterone release and some estrogen which prepares the endometrium for implantation by quieting it and:
- increasing blood flow
- increasing nuitrient secretions
- decreasing contractions of uterus
massive release of progesterone and some estrogen inhibits the FSH and LH release via GnRH inhibition via NEGATIVE FEEDBACK
if no pregnancy the CL begins to die (Cl needs FSH to LH to live and you have suppressed it so much through negative feedback there isn’t enough to support it) and the plasma estrogen and progesterone decrease, causes NECROSIS OF ENDOMETRIAL LINING AND NECROSIS
starting the cycle over with the increase if estrogen and progsterone in follicular phase
explain what happens in the luteal phase if fertilization occurs?
the blastocyst implants on the endometrial wall and forms placental membranes that secrete human choronic gonadotropin
HCG has a very similar structure to LH so it can therefore rescue the corpus luteum by binding with LH receptors
this means the PROGESTERONE PRODUCTION CONTINUES UNTIL WEEK 9-10 WHERE THE STEROID SYNTHESIS SWTICHES OVER TO THE PLACENTA
aka luteal-placental transition period
luteal phase defects
what does this cause?
2 things it can cause?
how does this happen?
inadequate secretory transformation of the endometrium
resulting from deficient progesterone production->contributes to both infertility and recurrent pregnancy loss
Causes:
- abnormal follicular development from inadequate FSH and LH
- causes inadequate growth of granulosa cells
- causes lower estrogen levels
- lower estrogen levels promote suboptimal LH surge at ovulation resulting in deficient progesterone in the luteal phase
exposure to estrogen can cause what?
increased risk of developing breast or uterine cancer since they stimulate proliferation of cells in both these tissue types
polycystic ovarian syndrome
what does this cause?
who is it common in?
what is the triad?
two additional considerations?
MC cause of infertility in women!!
often in adolescents
endrocine syndrome with triad of
(must have 2/3)
1. oligo (infrequent) or ammenorhea (chronic anovulation)
2. hyerandrodenism (obesity/hirsuitism)
3. evidecent of polycystic ovaries (not everyone)
thought to be caused or involved with increased insulin resistance** (increases the androgens) and **unopposed estrogen which increases risk for endometrial cancer since the person isn’t ovulating and there is no progesterone productionh
explain the hormonal interaction seen in polycystic ovarian syndrome?
7 steps
explain how this factors into exposure to unopposed estrogen exposure?
caused by an abnormal hypothalamus-pituitary ovarian axis
1. increased LH realeased compared to FSH
2. increase androstenedione and testosterone by the thecal cells of the ovary
3. androstienedione is converted to estrogen in the tissues, and is a weak estrogen
4. this STIMULATES LH release and inhibits FSH release
5. the low levels of FSH prevent the follciles from fully developing and ovulation doesn’t occur
6. the androstienedione that accumulates from the LH binding to the thecal cells continues to increase the androgen present cause HIRSUITISM and ACNE
7.this is a viscious cycle that cause anovulation and also the cystic formation of the ovaries
***INSULIN PLAYS ROLE BECAUSE IT IS THOUGHT TO CONTRIBUTE TO HIGH ANDROGEN LEVELS AND MAKE THE SITUATION WORSE!!!****
this explains why they are at risk for unopposed estrogens because since there is no ovulation (or corpus luteum development) there is no increase in progesterone which leaves the estrogen unopposed and increased risk for endometrial cancer!
polycystic ovarian syndrome
2 dx?
3 tx options?
DX:
- increased testosterone levels
- US
TX:
- OCP
first COC if contra then POP
treats hirsuitism and unopposed estrogen
- metformin for insulin resistance
- clompihene citrate for infertility-ovulation inducer
ovarian cysts general
what is it?
dx?
3 tx options?
how to prevent?
cystic enlargement of ovarian structures
DX:
US
Tx:
- fluid filled monitor with periodic US because most resolve on their own and ovary still functional
- if not fluid filled remove with laproscopic MC, remove is greater than 6 cm because increase risk of torsion
3.NSAIDS
prevention:
OCPS
follicular cyst
what is buz word?
sxs?
tx?
mc cyst type
“strawberry filled”
usually not sxs
resolve spontaneous
result from failure of ovulation so it doens’t produce a functional egg
corpus luteum cyst
when does this occur?
2 characteristics?
where does it develope
occurs after ovulation
thin walled and unilocular
developes withing the corpeus luteum
theca-lutein cysts in pregnancy or molar gestation
how large?
at risk for?
what does it often occur with?
3cm
at risk for multiple gestations
coinsides with molar gestation
molar gestation: there’s not true DNA developing but enough it develops like a fetus but it will never be viable and has teratomas and can develop outside of the uterus
hemmorrhagic cyst
what is the nickname for this?
why does this occur?
“chocolate cyst”
piece of endometriosis goes to the ovary and called this because of the accululation of blood and is messier if itruptures
what is the most LETHAL GYN cancer? what the nickname?
Ovarian cancer!
“silent killer”
by the time we dx it it is already really progressed and metastisizes!
if you find an enlarging ovarian mass with a solid component or change in character esp in post menopausal woman, what should you do?
REMOVE IT!! ASAP!!!
is it reccomended to screen for ovarian cancer?
no because it does not appeare to reduce mortality
what are the genetic markers associated with ovarian cancer?
CA-125
BRCA1 and 2
what is the most common type of ovarian cancer?
epithelial carcinomas
85-90% of all ovarian cancers
what are the 3 types of ovariance cancer classifications?
include caracteristics of each
5
4
4
1. epithelial
MC TYPE
most are benign
- epithelial carcinomas 85-90% of all ovarian cancers
- clear cell-rarely benign
- transitional
2.** **germ cell
occurs in cells that produce eggs
young women teenage-20s
5-10%
teratomes or dermoid cysts are in 40-50% and can contian hair and teeth
3. stomal carcinoma
in connective tissues of the ovaries that produce estrogen and progesterone
rare
low grade
produce hormones
what are 4 protective factors of ovarian cancer?
OCP
more than 1 full term pregnancy before age 35
breast feeding
tubal ligation
what percent of women experienced at least one sxs of ovarian cancer during the year prior to dx?
83% of women…so pay attention!
if ovarian cancer only accounts for 2.4% of cancer, why do we worry about it so much?
it is dx in late prognosis! so it kills a lot of people
“silent killer”
how much does have the BRCA1 and BRCA2 genes increase womens chance of ovarian cancer? what should they consider?
increase lifetime risk by 25-50%
***consider prophylactic billateral salpino-oophorectomy (BSO) by age 35 or as SOON as childbearing is complete for familial ovariance cancer syndrome!!!!!****
what are 6 RF for ovarian cancer?
- BRCA1 BRCA2
- 65-75 years
- early menarch, late menopause
- french canadians
- never being pregnant
- obesity
ovarian cancer
what are the 3 sxs that are likely to present in late dxs?
what do you need to keep in mind?
2 dx?
usually asymptomatic until late disease
late stage sxs usually when person presents
1. abdominal pain/bloating
2. early satiety (feeling full)
3. urinary urgency/frequency
palpable ovary needs evaluation!!!
dx:
- transvaginal US
- laparoscopic evaluation
what is the 4 tx options for ovarian cancer?
- surgery-removal of tumor (may be total hysterectomy)
- oophorectomy
- chemotherapy
- sometimes radiation
what is the 5 year survival rate for all stages of ovarian cancer? depends on? whats the key?
45% 5 year survival rate
highly dependent on stage of dx
**EARLY DETECTION IS KEY: survival increases to 75% if detected before leaving ovary!!**
low risk HPV causes:
high risk HPV causes:
low=genital warts
hight=cervical cancer/genital cancers
pap interpretation:
abnormal pap:
atypical sqaumous cell of undetermiens significance
ASC-US
2 age brackets and their perferred method of intervention
women over 25:
do HPV testing, if + go to colposcopy if - repeat cotesting in 3 years
21-24 year olds
repeat in 1 year
pap smear results:
abnormal pap:
low grade squamous intraepithelium lesion
LSIL
2 tx groups!
over 25
perform HPV cotest if positive do colposcopy, if negative restest in 1 year
age 21-24
repeat pape in 1 year, if above LSIL then colposcopy, if not continue guidelines
pap results:
abnormal:
acute squamous carcinoma-can’t exclude high grade
(ASC-H)
high risk of carcinoma
colposcopy for ALL no matter HPV status
pap smear results:
abnormal pap:
High grade squamous intraepithelium lesion
(HSIL)
2 age groups?
intervention for each?
correlates with CIN II or III at least
25 and over
colposcopy OR immediate loop electrosurgical excision LEEP
12-24 year olds
colposcopy ONLY
pap results:
abnormal pap:
atypical glandular cells
(AGC)
2 tx?
correlates to?
colposcopy
PLUS
endometrial sampling if over 35 or at high risk for endometrial cancer
for your reading pleasure
breast pain
“mastalgia”
what is this?
when is it more common?
what are the two differnt types and their characteristics?
3
3
what tests do you do for each?
MOST COMMON BREAST COMPLAINT IN PRIMARY CARE
premenopausal more common than post menopausal since often cyclic, and increases in women taking OCP or hormonr replacement
Non-cyclic
women 40-50
sharp burning pain
unrelated to mestruation
brest exam AND US ADD MAMMO if over 30
cyclic
heaviness soreness
billaterall, MC in upper outer quadrant
associated with hormone chages, usually 1 week prior to menstration (because the breast tissue proliferates
breast exam, US, add mammo if over 30
what are the 6 tx options for mastalgia?
- usually self limited
- support garments
- compresses
- analgesics
- evening primrose
- danazol only Rx for mastalgia but lots of SE
T or F: breast pain is rarely cancer?
TRUE!
nipple discharge
what are 3 causes? characteristics?
2
1
2
usually benign
- normal milk production
a. normal secretory milk
b. occurs 6 months after cessation of breast feeding - galactorrhea
a. caused by hyperprolactinemia, causing bilateral milky nipple discharge - pathologic (suspicious)
a. secretion of other fluids other than milk
b. most common cause is papilloma (papilloma tumor growing from the lining of the breast
if someone has pathologic nipple discharge what 5 sxs might they have?
- spontaneous
- unilateral
- bloddy, clear, yellow, white, dark green (LOTS OF COLORS)
- associated with mass
5. women over 40
if someone has benign nipple discharge, what are 3 potenital sxs?
- discharge with compression only
- often bilateral
- clear, yellow, dark green
what must you do for ANY breast lump?
exclude cancer!!!!!!!!!
this is 2nd most common breast complain in primary care, 90% are benign but still need to rule out cancer!!!
what is the triple test used when a breast lump is identified?
- breast exam
- mammorgram (often with US)
- needle BX
A. fine need aspiration (FNA)
B. core needle Bx (CNB)
how do you make a definitive dx of breast cancer? (3)
bx via…
- fine needle aspiration
- core needle bx
- open bx
what is the most common cancer in women?
breast cancer!
where are the 7 MC mestastasis placed for breast cancer?
- lymph node
- muscle, fatty tissue, skin
- bone
- bone marrow
- liver
- lungs
- brain
what are 7 potenital sxs of breast cancer?
- lumps
- bumps
- skin changes
- dimpling
- red, hot
- pain/no pain
- regional node enlargement
what predominates in premenopausal women with bumps/lumps
benign conditions predominate
what predominates in post menopausal women with lumps and bumps? what do you need to remeber?
malignant lesions
in postmenopausal women, any dominant mass or assymetry should be presumed cancerous until proven otherwise
how do you determine between a mass and a cyst?
US!!!
sometimes simplest is to aspirate the mass
what should any solid mass, wheter or not it is imageable, warrants…
a definitive dx…bx it!!!
what is the GOLD STANDARD for dx breast cancer?
Biopsy!!! superior to even the most advanced imaging
when in doubt when it comes to a mass…
assume nothing!
aspirate or refer to surgeon
Malignant neoplasm:
Pagets disease
what is this?
common?
what are two other things to look for?
5 sxs?
cells collect around the nipple causing eczematous appearance
Rare-5%
97% also have ductal carcinoma in situ OR invasiver cancer elsewhere in the breast
sxs:
ITCHING
TINGLING
BURNING
scaling and thickening of the skin
yellow or bloody discharge from the nipple
non-invasive breast cancer:
ductal carinoma in situ
what is this?
common?
life-threatening?
how are they found?
2 tx options?
MOST COMMON TYPE OF NON-INSIVE BREAST CANCER
1 in 5, 25% of all BC is this
non-lifethreatening, typically without signs and symptoms
increases risk of developing invasive BC
80% found on mammorgram
tx:
- lumpectomy alone 25-30% recurrence
- lumpectomy and radiation 15% recurreny
non-invasive breast cancer:
lobular carcinoma in situ
what is this?
what does it increase risk of?
when/how is it dxed?
receptor positive?
collection of abnormal cells, not true cancer
increases risk of invasive cancer later in life
dxed before menopause, usually dxed becuase bx performed for some other reason
hormonal receptor positive
Breast Cancer:
invasive ductal carcinoma
what is this?
what percent?
6 sxs?
5 tx options?
most common invasive breast cancer!!!
70-80% of BC
SXS:
1. swelling of all or part of the breast
2. skin irritation or dippling
3. breast pain
4. nipple pain/nipple turing inwards
5. nipple discharge other than milk
6. enlarged lymph nodes in the axilla
TX:
- lumpectomy less than 2 cm
- mastectomy (partial, total, radical)
- sentinel lymph node bx
- axillary lymph node bx
- post surgical radiation
what is involved in pt follow up for invasive ductal carinoma breast cancer?
4
- provider visit with exam every 3-6 months for first 3 years
- every 6-12 months for 4-5 years
- every year post 5 years
- yearly mammogram
what are 5 additional tx options for a patient with with invasive ductal carcinoma post lumpectomy?
1. chemotherapy
2. hormonal therapy
3. estrogen receptor down regulatiors-tamoxifen
4. oviaran shut down or removal
5. HER2 therapies-block HER2 that allows for rapid cancer growth
breast cancer:
invasive lobular carcinoma
common?
where does it occur?
age?
2ND MOST COMMON TYPE 10% OF CA
BEGINS IN THE MILK PRODUCING LOBULES
occurs later in life around 60s
invasive breast cancer:
inflammatory breast cancer
what does this look like?
how to dx?
4 staging options?
2 tx options?
rare, average age in 55s
looks like eczema on the breast (not confined to nipple), breast enlarged
DX:
- skin punch bx
Staging:
1. CXR
2. CT of chest/abdomen
3. bone scan
4.LFT
TX:
1. chemotherapy prior to surgery
2. targeted therapy: if HER2 receptor postivie also treat prior to surgery HECEPTIN
invasive breast cancer:
inflammatory breast cancer
how does your response to pre-surgical chemo effect the next step in tx?
if cancer response to first dose chemo before surgery: modified radical mastectomy
if no response to first dose chemo before surgery: another round chemo + radiation and likely radiation AFTER surgery
what are 7 RF in developing breast cancer?
- female
- greater to 55
- no children, no breastfeeding
- exogenous exposure to estroen
- family hx postive for BC 1st degree relative
- BRCA1 and 2
- obesity
BRCA1 and BRCA2
risk?
age?
where?
60% increase in risk of BC
- develope breast cancer earlier
- have bilaterally breast more often
do malignant breast conditions tend to have more or less discharge?
less
how do you dx breast cancer?
4
- yearly breast exam by provider
- US
- aspiration/bx=gold standard
- mammogram-controversial time frame
mammogram guidelines:
(2 main guidelines)
very controversial
2 main:
- start at 40, Q 1 or 2 years
- start at 50, Q1 or 2 years
how is Breast cancer staged?
3
- size
- spread to lymph node
- metastasis
when are 6 instances it is appropriate to test a patient for BRCA1 and BRCA2?
- eastern european
- AA before dx before 35
- in all family of man dx
- women with BC in both breasts
- multiple family with breast or ovarian cancer
- blood relative before 50
benign brest lump:
fibroadenoma
6 descriptive characteristics?
who common in? from?
dx?1
tx? 1
solid
round, firm, notender, mobile mass “rolled to and edge”
TYPICALLY IN YOUNG woman 15-35
likely from hormones
DX:
core needle bx
TX:
excision
fibrocystic disease
4 descriptive words?
who common in?
pain type?
asspcoated with what?
2 presenting complaints?
2 dx?
1 follow up?
diffuse/ill-defined, TENDER
fluid filled mass MC in premenopausal, cyclic breast pain
OFTEN ASSOCITED WITH HORMONAL CHANGES, AND CAN CHANGE IN SIZE WITH MENSTRUATION
presenting complaint: pain/palpable mass
DX:
- US
2. fine need aspiration for confirmation
3. CBE or US in 2-4 months following aspiration to document stability
galactorrhea
cause?
billateral, milky nipple discharged caused by hyperprolactinemia
gynecomastica
what is this?
ages?
3 things found on PE?
tx?
benign proliferation of glandular tissue in male breast
neonatal, pubertal, older males due to increased estrogen and decreased androgen
PE:
palpable mass over .5 cm (usually under the nipple)
NONTENDER,
FIXED
TX:
usually self limited
what are 5 pathologic causes of gyncomastica?
- drugs
- cirrhosis
- hypogonadism
- tumors
- CKD
mastitis
what is this?
when is it likely to occur
causaitive agent?
4 PE?
tx? 2
inflammation and pain of the breast, most frequently occuring during breastfeed from infection with staph aureus or strep
MC: staph!!!
if left untreated can become an abcess!!
PE:
- hard, red
- inflammed tender area of breast
***since infection blocks off the duct and it becomes backed up, and at increased risk from breastfeeding since there are more cracks from suckling***
tx:
DICLOXACILLIN or CLINDAMYCIN (MRSA)
breast abcess
from?
tx?
can be a complication of mastitis and required incision, drainage, and abx
what STI has the highest prevalence?
HSV
what STI has the highest incidence?
HPV
how many new STDs are there annually in the US?
19 million
what are 6 complications you see with STIs?
- infertility
- ectopic pregnancy
- low fetal birth weight
- chronic pelvic pain
- cervical and angogenital cancer
- HIV transmission
who is at greatest risk for STIs?
youth
50% are in those 15-25 year olds
what do you need to do if a patient has either gonnorhrea or chlamydia?
tx as if they have both
how much greater is the risk of HIV if you have a STI? why?
2-5x greater risk!!
STIs attract CD4 cells to the genital area, so when infected with HIV they are already there. some STIs cause ulcers and therefore also create a portal of entry
by treating the STI you reduce risk 40%
gonorrhea
what bacteria?
4 things it effects?
hallmark?
Men 2 sxs
women 2 locations, 4 sxs
ANOTHER OPTION FOR INFECTION
neisseria gonorrhoae
effects cervix, urethra, rectum, pharynx
“Mucous membrane dxs” of men, women, babies
antibiotic restisance is hallmark
men
1. urethral discharge (thick, milky white, yellowish, or greenish)
2. swollen or tender testicles (epididymitis)
women
endocervical or urethra
- majory asymptomatic
2. vaginal discharge, dysuria, labial pain/swelling
3. pain during sex
****DISSEMINATED GONOCOCCAL INFECTION***
SXS
- arthritis-tenosynovitis
- cutaneous and along tendon sheeths
gonorrhea in infants
2 causes
mother can trasmit during child birth
caues:
sepsis
opthalmia neonatorum
what are 6 RF for gonorrhea?
- <25 years
- previous C/other STDS
- commercial sex work
- mew or multiple partners
- inconsistent condom use
- drug us
what testing do you use to dx gonnorhea in men and women? collection method?
NAAT
*make sure to monitor abx susceptibility*
collection method
WOMEN: vaginal swab
MEN: dirty urine sample
what is the tx for gonorrhea?
2
3 drugs each
DOC1:
ceftriaxone 250 mg IM single dose +
(azithromycin OR Doxy)
DOC2: only if ceftraixone not avaliable
cefixime +
(azithromycin or doxy)
what are 3 complications a woman can get from gonorrhea?
1. bartholins cysts
2. pelvic inflammatory disease
3. disseminated gonnocooccal infection
what do you need to make sure you do when txing for gonorreah?
restest woman/men in 3 months after tx
chlamydia
what bacteria causes this?
what can it cause? 4
sxs in women? 4
sxs in men? 4
chlamydia trachomatis
cervicitis, urethris, proctitis, PID
men, women, children
women
usually asymptomatic
mucopurlulent cervicitis, red and hot
abnormal vaginal discharge
pain during sex
men
usually asymptomatic
discharge from the penis, may be running, whiteish, thin
burning on urination
swollen testicles, epididymitis
chlamydia
how do you dx and collect in M/F?
what si the DOC1?
DOC2?
DX:
NAAT
urine test: men
vaginal swab: women
TX:
DOC1: azithromycin 1 g once
DOC2: doxy 100 mg BID x 7 days
do you need to bring people back in to be rested after tx for chlamydia?
ONLY IN PREGNANCY
**wait 3-4 weeks to restest so the DNA from the dead bacteria doesn’t produce a a false positivie**
expidited partner therapy
what is it?
txing sex partners without a visit…rules still being written in maine.
**can legally write prescription for partner if they aren’t youre pt so tx increases**
herpes simplex
what is a hint that an outbreak is going to occur? what is the important description of these? what are the two different types; where are they found and what percent of the population has them? how do you dx it and what do you see? what are the four treatment options?
prodromal phases: 24 hours before outbreak, get burning and tingling
“painful grouped vesicles on erythmatous base!”
HSV1: oral lesions 85% population infected; transmitted via saliva, outbreak triggered by random things
HSV2: genital herpes (more common and detrimental in women! more likely to have complications like ulcers and necrotic tissue), 25% population infected
DX:
- clinical for the most part
2. tzank smear, geimsa stain shows GIANT MULTINUCLEATED CELLS, can also check for antibodies for this via PCR
TX: supportive therapy
suppressive therapy
Acyclovir, valacyclovir, famcyclovir
acute hepetic gingivostomatits
what virus causes this? where does this tend to effect? how often are the outbreaks and who are they common in? what are three things you might find in this patient? explain the maturation of the vesicles?
HSV-1-trigeminal nerve predilection, eruptions 2x a year
common in 6 months-5 years CHILDREN
abrupt onset fever, anorexia, red mucosa
vesicles appear on gums, lip, tongue
vesicles colase to form ulcers or plaques
acute herpetic pharyngotonsillitis
what virus causes this? who is it the most common in? what are four symptoms you see with this? what do the lesions look like?
more common in HSV1 than HSV2
primarily in ADULTS
fever, malaise, headache, sore throat
vesicles on posterior pharynx and tonsils that RUPTURE to form ulcers (may have grayish exudate)
what are the 5 complications you worry about from herpes simplex virus?
1. herpetic withlow (vesicles on the fingers)
2. herpes gladiatorum (disseminated cutaneous infections common ing wrestlers)
3. keratoconjunctivitis (dendritic corneal ulcers)
4. HSV or CNS ENCEPHALOPATHY!! YIKES!! causes change in mental status and headache
5. infection during pregnancy can infect the child
what is herpetic whithlow?
herpes lesion on the FINGERS
Herpes Simplex-2
what does this cause? what percent of the population is infected with this? where does this typically have predilection for? what do the lesions start and finish as? what percent of people will have reactivation in the first 12 months? how many reactivations will they have in their lifetime?
causes genital lesions
25% of the population infected with this
asymptomatic shedding and painful eruptions can occur
sacral root ganglion predilection
VESICLES rupture to form ULCERS
reactivation in 90% occur in the first 12 months!!
30% have 6 episodes in their lifetime!!
where does Herpes simplex virus tend to hide?
dorsal root ganglion
this is why it reactivates
acute cervicitis
4 characteristics
5 potenital pathogens
purluent vaginal discharge
usually infectious
risk of PID if not treated
sometimes post-coital bleeding
comon pathogens;
- gonorrhea
- chlamydia
- candida
- bacterial vaginosis
- trichomonis “strawberry cervix”
chronic cervicitis
main sxs?
infectious?
4 sxs?
3 tx?
leukorrhea main sxs
noninfectious
dyspareunia
dysmennoreah
low back pain
urinary sxs
Tx:
- cryrosurgery
- laser
- electrocautery
syphilis
bacteria?
transmission requirements?
more common populations?
when does most transmission occur?
explain progression phases? 6
treponema pallidum
spirochete bacterium
transmission: vaginal, anal, oral through contact with syphilis chancre, and requires contact with open lesions to spread
More common in MSM and AA
30% occurs during the early or secondary phases
early
primary
secondary
early latent
late
latent
tertiary
neurosyphilis
early:
primary syphilis
what is the hallmark of this? 2
where does it go next? fast?
- chancre at site of innoculation thats NOT PAINFUL
- heals spontaneously
- quickly becomes systemic
- spreads to local lymph nodes
- dividing time of 30 hours
early:
secondary syphilis
when does this occur?
in what percent?
4 findings?
2 additional related findings?
weeks to months after initial infection (25% of untreated)
SXS:
1. RASH MOST COMMON (can be on palps, and soles!!!!)
- fever/malaise
- annorexia
- diffuse LAD
Additional findings:
1. condyloma lata
-war like lessions in the genital area
2. patchy alopecia
-“moth eaten appearance
late:
latent syphilis
what is this marked by?
infectious?
tx?
totally asymptomatic past 1 year, marks this time
1. slower metbolism of bacteria and prolonged dividing time
- thought to be non infectious
- requires longer tx
early:
early latent syphilis
what is important about this stage?
S&S
time frame?
infectious?
infection demonstrateble by serologic testing with Treponema pallidum
NO SIGNS OR SYMPTOMS
1 year or less
potentially infectious
late:
tertiary syphilis
what are 2 things that mark this?
1
3
when does this occur?
- gummas!! (nodular tumor like growths)
- cardiovascular
- aortitis MC
- aortic aneurysm
- aortic regurg
1-30 years after initial exposure
may never have had clinicallly apparent primary or secondary
late:
neurosyphilis
what are 9 presentations of this?
general paresis of the insane
1. personality change
2. hyperactive reflex
3. argll-robertson pupils
4. sensory deficits
5. tabes dorsalis shuffling gate
6. opthalmic involvement
- uveitis
- neuroretinits
- optic neurtis
7.auditory sxs
8. cranial nerve palsies
9. meningitis sxs
congenital syphilis
transmission to stillborn
90% result in stillborne
HUTCHINGSON TEETH
How do you dx primary/secondary syphilis?
4
- nontreponemal test
screening for reactivity to cardiolipin-cholesterole-lecithin
RAPID PLASMA REAGIN with titer
- treponemal test
CONFIRMATORY
detects antibodies against treponemal cellular components, QUALITATIVE
- multiplex PCR
**neurosyphilis must do CSF analysis**
penile cancer
what type of cells?
tx?
squamous cell origin
“something doesn’t look right”
TX: surgical
how do you tx early stages of syphilis?
includes primary, secondary, and early latent
DOC1: penicillin G benzathine 2.4 million units IM
DOC2: doxycycline
how do you tx late latent syphilis?
DOC1: 3 shots of 2.4 million penicillin G beenzathin IM over 3 weeks
DOC2: doxy PO for 4 weeks
how do you tx tertiary syphilis?
Penicillin G 2.4 million units IM weekly for 3 weeks
how do you tx neurosyphilis?
penicillin G 3-4 million units IV Q4
OR
24 million units IV over 10-14 days
treating sex partners of those dxed with syphilis?
3 options
- if patient in early stages
A. partner exsposure within 90 days TREAT PRESUMPTIVELY
B. partner exposure over 90 days TREAT PRESUMPTIVELY if no test avaliable or partner followup unlikely, otherwise ok to tx by evaluation
- if patient in late stages
evaluate partner clinically
- if pt stage unknown approach same as early
what is a strange rxn you should know can occur when txing a patient for syphilis
jarish herxherime rxn
occurs within 24 hours
fever, HA, myalgia
can cause early labor or fetal distress
*****what do you need to test patients with syphilis for???****
NEED TO TEST ALL PATIENTS WITH SYPHILIS FOR HIV!!!!!!
MUST ALSO RETEST IN 3 MONTHS in high prevalence areas!!!!
bacterial vaginosis
what is this?
3 sxs?
how dx?
1 tx?
controversy if it is an STD or not because it is an overgrowth of the patients own flora, however it rarely occurs in women who aren’t sexually active
sxs:
1. malordorous white/grey discharge
2. pH greater than 4.5
3. absence of dyspareunia
DX:
CLUE CELLS-cells covered in coccibacilli
**don’t do culture of this, just a wet moutn because it ths the womans own flora so the lab will just show that
TX:
METRONIDAZOLE 500 mg BID x 7 days!!
why do we care about txing bacterial vaginosis?
8
- increased risk of preterm birth/rupture of membranes
- amniotic fluid infection
- postpartum endometriosis
- PID
- postsurgical infection
- cervical intraepithelial neoplasia
- mucopuruloent cervicitis
- acquisition of HIV infection
blantitis
who do you find this in?
what is the typically cause?
2 tx?
“acorn infection that is like vaginal yeast in women”
infection of the head of the penis usually fungal
often seen in uncircumsized men
TX:
- OTC antifungals like monistat or oral fluconazole
trichomoniasis
what is this?
5 sxs?
3 dx methods
tx1?
flagellated protozoan
SXS:
1. pruritis
2. malordorous, froththy, yellowgreen discharge
3. could have erythema around vagina
4. dyspareunia
5. post coital bleeding
dx:
1. wet mount show motile flagellates
- amine test positive
- pH 5-6
Tx:
METRONIDAZOLE in single 2 gram dose
trichomoniasis:
what do you need to do for all sex partners?
treat them!
hydrocele
what is this?
2 ways to dx?
2 tx options?
water on the testicle from congenital remnants of the tunica vaginalis
a soft, nontender fullness of the hemiscrotum that transillumates
dx:
1. us
2. transillumination
tx:
1. usually reassurance
2. hydrocoelectomy
explain how the parasympathetic and sympathetic system control and erection?
parasympathetic: engorgement of the copora cavernosa
sympathetic control: contraction of SM and ejaculation
hypospadius
what is this?
what are two adaptations this person might have
3 locations?
tx?
urethral meatus is no present at the tip of the glans
a midline defect
male may need to sit for urination and may cause issues with ejaculation
optioins:
- subcoronal (beneath glans
- midshaft
- penoscrotal
Tx:
sometimes requires correction
peronies disease
what is this?
4 tx options?
rigid scarring of the penis resulting in a crooked, painful erection
unknow etiology
TX:
- injection verapamil
- radiotherapy
- surgery
- shock wave therapy
prostadynia
pain without infection….tx with NSAIDS
what is the name of the new drug that is used to tx overactive bladder?
beta-3 adrenergic
MIrabegron
that relaxes the SM
if a person has both BPH and ED…what drug do you want to give them?
tadalafil (cialis)
how often should DRE be preformed?
begin at age 50 if life expectancy is 10+ years
compare the curability of testicular cancer and prostate cancer?
testicular cancer is very curable where prostate cancer isn’t
epididymitis/orchitis (testes)
what are the two MC causes of this for the different age groups?
how does this present?
what sign is pos?
2 dx?
2 tx options?
younger less than 35: MC chlamyida
older than 35: MC gram neg bacilli, E.coli
sudden onset of unilateral top of the testicle pain and swelling often caused by secondary infection from reflux of urine
***Prehn sign positive: relief of sxs with elevation of the scrotum***
DX:
US
UA
TX:
1. E. coli: ciprofloxacin
- chlamydia/gonnoreah: azithromycin + ceftriaxone
prostatitis
what is the difference between acute and chronic?
SXS? 5
2 dx?
2 tx?
ACUTE:
often in young, with sudden onset
often e.coli, klebsiella (poop bugs)
CHRONIC:
prostate normal on exam
can be from reccurent infection or inflammation
SXS:
- FEVER CHILLS
2. PROSTATE TENDERNESS
3. DYSURIA (SINCE INFECTION!)
4. URINARY FREQUENCY
5. LOW BACK PAIN!
DX:
- consider prostate massage if first culture negative
- clinical and UA
Tx:
- ciprofloxacin
- alpha blockers
testicular torsion
what is this and what are you at risk for?
who is most likely to get this? esp?
emergency? 3 sxs?
testes is anormally twisted in the spermatic cord thus comprimising arterial blood flow and venous drainage which leads to testicular ischemia
most common in prepubertal and post pubertal 12-18 year old males, esp with those who had crytorchidism or late decent of the testes
UROLOCIAL EMERGENCY!!
SXS:
- negative prehns sign-no relief with elevation of the scrotiom
2. unilateral, swollen, retracted testicle
3. absent cremaster reflex
testicular torsion
2 dx?
3 tx?
DX:
- clinically
- doppler US shows decreased blood flow
TX:
- NSAIDS
- surgical detorsion and orchiopexy (make teste descended)
***GOAL: GET THIS ALL DONE WITHIN 6 hours!!!***
phimosis/paraphimosis
what are these?
who are they common in?
tx?
phimosis: can’t readily retract the foreskin to the corona or the glans “turtle stuck inside”
paraphomosis: tight forskin around the base of the glans so “turtle head can’t go back in”
common in uncircumsized men
TX:
circumcision!! TOC
benign prostatic hyperplasia
who does this happen in?
where does it start in response to what?
what does it cause?
7 sxs!!!
increased incidence in nearly ALL MEN!!
80 and up 90% incidence!!!
begins around the urethra in response to increase dihydrotestosterone production and estrogen causing
urinary obstruction leading to SXS
SXS:
1. decrease in stream quality
a. hesitancy
b. dribbling
c. takes longer to pee, don’t pee as far
2. incomplete emptying/frequency
3. retention
4. nocturia
how are symptoms for BPH scored? 2
international prostate symptom score (IPSS)
American system (AUA)
what are the 3 general tx options for BPH?
- watchful waiting
- medications
- surgery
**depends on severtiy of sxs!!***
what are 3 tx options for BPH?
how do they work?
any cautions?
3
- alpha 1 adrenergic blockers “flow”
“TAMULOSIN”
relax bladder to improve sxs
***watch for decreased libido, dizziness, floppy iris syndrome***
- 5 alpha reductase inhibitors “shrink”
“FINASTERIDE”
inhibit enzyme that convert testosterone to 5 alpha dihydrotestosterone (DHT) which decreases testosterone stimulation of the gland
- combination-increase flow and shrink
- dutasteride/tamulosin
- tadalafil
what is a strange non pharmaseutical that works for BPH?
phytotherapy with saw paletto (palm tree extract)
what are the 4 surigcal options for BPH?
- transurethral resection of prostate (TURP)
- transurethral microwave therapy (TUMT)
- transurethral needle ablation (TUNA)
- transurethral US guided laser induced prostaectomy (TULIP)
do you always tx BPH?
no! only if pt is symptomatic
varicocele
what is this?
where?
what does it feel like?
P&P?
DX?
TX?
dilation or vericose spermatic veins usually on the left with bag of worms feeling
sxs:
- non tender mass without transillumination
- increases in size with valsalva
3. decreases in size with scotal elevation
DX:
- doppler US
TX:
surgical repair via vein ligation only if paiful or preventing fertility
testicular cancer
who is this most common in?
what are the two types?
3
1
2 main presentations?
typically in younger men 20-40 years old
- seminoma tumors
a. less aggressive
b. radiosensitive (get radiation tx)
c. normal levels
******seminoma are Simple and Sensitive*****
2 non-seminomatous tumors
a. screte AFP but not HCG (green book says both
sxs:
painless testicular nodule, solid mass, or enlargement “heavy testicle”
what puts a person at higher risk for testicular cancer?
cryptochidism
(undescended testicle)
what is the cure rate for testicular cancer?
90%
testicular cancer
3 dx
3 tx
dx:
1. US
2. Self exam/physical exam
3. tumor markers
beta human gonadotrophic hormone (beta HCG)
alpha feto protein (AFP)
tx:
- orchioplexy-CUT IT OUT
- chemotherapy
etoposide +cisplatin+/-bleomycin
- fix cryptochidism before puberty
if someone is dx with testicular cancer, what MUST you do?!
you must get a chest xray because testicular cancer metastasizes here!
prostate cancer
where does this occur?
invasive?
sizes of prostate?
screening?
occurs in the secretory gland below the bladder that contributes to seminal fluid
common, slow growing cancer that leads to urinary obstruction“you die with it not from it!!
Prostate
usually 20 ml (chesetnut or walnut)
prostate cancer: 40 ml enlarged golf ball
Need to make sure to screeen since hereditary!!!!
prostate cancer staging!**
what do you use to stage?
explain the rating system
gleason scoring
1= well differentiated (favorable)
5=poorly differentiated (unfavorable)
THEN
add the two bx together for a score between 2-10, 10 is the worst oucome
what are the sxs with prostate cancer? 2
how do you dx? 3
sxs:
usually asymptomatic untill metastsizes to bone causing bone pain
might cause urinary sxs if gotten into uretha and cause
dx
- DRE: hard irregularity/nodule, usually posterior
- transrectal bx or US guided bx
- if positive get erdionucleotide bone scane to look for metastasis
where are the 4 places prostate cancer likes to metastasize?
- bone
- blood
- lymph
- local
how can you screen for prostate cancer? 3
controversial
- DRE
- PSA
- prostate cancer antigen 3
who has the highest incidence for prostate cancer? general lifetime risk?
african americans
general lifetime risk: 16%
what are the 4 tx options for prostate cancer? what is the gold standard?
- surgery-radical prostatectomy or robotically
a. can cure
b. high incidence of impotence and incontinence
2. radiation with external beam or implantable seeds
a. not curative
b. palliation of bone mets
c. less impotence and incontinence than surgery
3. hormone-androgen deprevation
a. suppressive, not curative
4. chemo? not effective as much
what are you options when using hormone therapy for prostate cancer and androgen deprivation? what drugs can you use for each method?
- remove testosterone production via orchiectomy (remove teste)
- inhibit ACTH and estrogen (leuprolide)
- inhibit testicular synthesis of testosterone (aminoglutethimide)
- inhibit binding of androgen (flutamide)
prostate specific antigen
what is this?
1 pro
2 cons
controversial?
serine protease that is involved in liquefaction
pros:
elevated in 65% of cases
Cons:
35% false negative rate
non specific since also raised in prostate enlargement and prostatis
leads to more dx but doesn’t decrease mortality so controversial…why look for a problem?
psychogenic causes of erectile dysfunction
what percent of cases?
what is this?
2 common causes?
3 problems seen
20% of cases
common cause and occurs because the mood must br right, commonly effected by depression and anxiety
Problems seen:
1. can’t initiate
2. can’t fill (encgorge) usually arterial proble
-diabetes
-HTN
-ASHD
3. can’t store veno occlusive dysfunction
organic causes of erectile dysfunction
what perecent of cases is this?
4 causes
3
2
1
1
80% of cases
causes:
1. hormonal
-loss of testosterone in testicular failure
-pituitary tumor producing prolactin
-pituitary failue
2. drugs
-antihypertensives
-psychological
3. vascular disease
4. peyronies disease
what is premature ejaculation in origin?
what can be used to help this?
psychological in origin
SSRis like fluoxetine might help
priaspism
what is it what do you do?
persistent painful erection
emergent urology consult
what is the difference between primary and secondary hypogonadism?
primary
low testosterone, high LH or FSH (north works, south doesn’t
secondary
low testosterone, low to normal LH/FSH, so therefor north not working well too
what testing sequence should you do to evaluate for hypogonadism?
- AM total testosterone level
- if low, repeat morning testosterone x2
Interpreation:
A. if low testosterone, with LH and FSH not elevated then it is secondary hypogonadism
B. if low testosterone, with increased LH and FSH than primary hypogonadism
what are 5 test you want to do for erectile dysfunction?
1. testosterone level
2. prolactin levels **if this is high, it causes low levels of testosterone**
3. LH
4. US
5. nocturnal penile tumescence testing “tape testing”
if prolactin levels are high what do you want to do?
get MRI because it likely has CNS origin, possibly tumor
what are 5 tx options for erectile dysfunction?
what does the medication do?
what can it cause?
effected by?
2 names?
- replace testosterone if low
- phosphodiesterase 5 inhibitor
- relaxes SM allowing for filling
- can cause headaches and flushing and when combined with nitrates can cause massive dip in BP
- effected by high fat meanls
SILDENAFIL/TADALAFIL
- prostaglandin E1
- alprostadil
- intra-penile injection or intraurethral - vaccum device
- surgery-penile prosthesis
what is hypogonadism caused by? how to you give testosterone?
- testicular failure
- problems from hypothalamic/pituary axis
**give depo-testosterone IM 1-2x a month!!**
cryptochidism
who does this occur in?
what is this?
2 RF?
consequences if not fixed?
1 PE finding?
1 Tx option
one or more undescended testes that don’t move into the scrotal sac, which remain in the abdomen or stuck in the inguinal canal
**those born prematurely or are small for gestational age have he highest risk of effect**
consequences:
1. infertility
2. testicular torsion
3. maligancy
PE:
- absence of palpable testicle, or palpable within the inguinal canal
TX:
- SURGERY! by age 1 to prevent risk of infertility
what does having cryptorchidism increase your risk for?
increases risk of malignancy in undescending testis is 4-10 times greater than gerneral population
what is parturition?
encompasses everything having to do with birth
birthing, prelude to labor, prep for labor, actualy labor process, initial recovery from childbirth
what are the 4 things that initiate labor?
- progesterone withdrawal
- fetal lung maturity
- fetal adrenal glands
- oxytocin release
what are the 9 hormones that play a role in parturition?
estrogen
progesterone
oxytocin
HCG
prostaglandins
LH
relaxin
corticotropin-releasing hormone
parathyroid hormone related protein
FIRST STAGE
what are 5 things this stage is marked by?
body changes?
how long?
stages?
5 things youre doing?
- cervical dilation 0-10 cm
- longest stage
- 7-14 hours
- early/late, active transition
- normal first stages eval
a. monitoring mother
b. monitoring fetus
c. body care of woman
d. supportive care for family
e. screening for complications
second stage of labor
dilation of what?
how long?
what are you doing?
what to be concious of during this phase?
- 10 cm to birth of baby
- 1-3 hours avg
- this is when your push
- fetal and maternal adverse outcomes occur during the second pahse of birth!!
how long does it take to push out the baby during the second phase of birth?
nulliparious woman
1.1-2.9 hours, 3.6 hours with epidural
multiparous woman
.39-1 hour, 2 hour with epidural
***hence women who are multiparous take less time to have a child***
third stage of labor
how long does this take?
what happens here?
what are 4 things that occur?
- birth and delivery of placenta
- 10-15 minutes on avg, up to 30
- uterine contractions
- uterine fundus at level of umbilicus
- “folding of placenta at implantation site
- formation of hematoma between placenta and decidua
what does the bishop score tell you?
the bishop score tells you how likely it is for succesful induction or compense spontaneously
score of 8+ is relatibly predictive of succesful induction
what are the four phases of uterine contraction?
1
1
0
4
phase 1:myometrium quiescence (rest)
occurs for 95% of the pregnancy
phase 2: uterine awakening
contractions and cervical softening via collagen fibers
phase 3: active labor
phase 4: maternal recovery
a. uterine involution
b. cerical repair
c. breast feeding
d. restoration of fertility
uterine contractions
what are the 5 anatomical changes that are occuring?
- compression of nerve ganglia in cervix
- stretching of the cervix
- hypoxia of contracted myometrium
- stretching of the perioneum overlying the fundus
- uterine actitive
- actively contracting upper segement becomes thicker and firm and doesn’t relax so it continually pushes baby out
- lower uterine segment and cervix become softer distended and mroe passive as labor occurs
what can the initiation of labor be marked by?
increase in vaginal discharge that is blood tinged
what are two changes to the cervix you see to prepare for labor?
- cervical dilation
- effacement (shortening and thinning)
what are 6 things that might mark the begining or getting closer to labor?
- lightening 2 weeks before-breathe easier
- cervical changes yielding ripeness
- false labor (can go on for days)
- permature rupture of membranes 80% of women will begin labor within 24 hours
- bloody show 24-48 hours before onset of labor
- gastrointestinal upset ie vomiting diarreah
what cervix dilation is marked as usually the begining of the active phase of labor?
6 cm appeares to be the landmark for the start of the active phase
what are 3 tests you use to determine if T/F labor, or postion of baby? what are 4 things you use to classify this?
- sterile vaginal exam
EFFACEMENT
DILATION
STATION
distance between fetal presenting part and ischial spine
- leopolds maneuvers
- US
use this to determine lie, presentation, position and variety
Baby:
lie
transverse, longitudal
baby:
presentation
3
cephalic (head down)
breech (butt down)
shoulder
baby:
position and variety
occiput/vertex (want)
siniput/military
brow
face
at what point is it pivitol the baby is cephalic?
34 weeks because before them babies move around a lot so not as worried about it
if breeched, what is the most succesful vaginal delivery that some placed will allow?
frank breech
what are the 3 P’s that determine if the birth is going slower than expected?
- passanger (size/position)
- pelvis or passage
- power (uterine contraction)
maternal dehydration
maternal exhaustion
uterine insuffieciency
what are 7 options for pain mangement for labor?
- stadol
- nubain
- demerol
- fentanyl
- nitrous oxide
- epidural
- morphine: long labor lasting longer than 2 days
where does a epidural block? what must you consider?
3 risks
L4 to toes
- reduced mobility
- longer labor
- must weigh with risks
-epidural fever
-maternal hypotension
-fetal distress
what are the 7 cardinal movements of labor?
- decent, flexion, and engagement (all together)
- internal rotation
- extension of the head
- external rotation of fetal head
- expulsion
placental separation
timing?
normal blood loss?
abnormal blood loss?
4 traditional signs?
15-20 mins, sometimes 30
Normal blood loss: less 500
post partum hemm: over 500
four traditional signs:
1. lengthening of umbilical cord
2. uterus changes to more globular shape and becomes firm
3. uterus rises in abdomen-placenta descends
4. GUSH OF BLOOD OCCURS
what is the physiologica or active management of:
- uterotonic
- uterus
- cord traction
- cord clamping
what is the most common cause of maternal mortality in developed countries? percentage?
postpartum hemmorage
18%
what are the 3 options for fetal monitoring?
1. auscultation: fetoscope or dopple
2. external fetal heart monitor-continuous or intermittent
3. internal fetal heart rate monitor-fetal scalp electrode
what is the gold standard to make sure the membranes are intact?
ferning method
how often should you monitor the fetal HR in the first and second stage of labor?
every 30 minutes in active labor
every 5-15 minutes in second stage
is continuous external fetal moniting suggested?
NO! not according to the US task for! they say it increases the risk of c-section and unnessary use of forcepts and suction on children! increasing risk!
placental abruption
what is this?
what are 2 sxs?
dx
tx 2
life threatening for the fetus where placenta seperates from the uterus prior to delivery and blood pools behind the placenta
MC cause of late pregnancy bleeding
SXS:
vagina bleeding
abdominal pain
DX:
1.. US
TX:
if less than 36 weeks w/o distress: monitor in hospital
if fetal or maternal distress: deliver!! c-section!
what are risk factors for placental abruption?
8
- previous placental abruption
- HTN
- abdominal trauma
- substance abuse
- premature rupture of membranes
- blood clotting disorders
- multiple pregnancy
- maternal age-especially after 40
cesarean section
what percent of births occur this way?
what are the 5 most common causes of this?
birth of the fetus through an insision in the abdominal and uterine wall
1/3 of total births
Causes:
- repeat cesarean
- fetal intolerance to labor
- fetal position
- maternal emergency
- CPD
dystocia
wat is this?
3 causes to take into consideration?
4 tx options? when do yo uconsider them?
abnormal labor when the cervix fails to dilate progressively over time and the fetus fails to descend
causes
1. pelvis: passage through pelvis impaired
2. powers: inadequate contractions to dilate cervix and expel baby
-active upper portion with passive lower segement
3. passenger: cephalopelivc disproportion, malpresentations and malpositions
TX:
1. oxytoxin/pitocin to induce contraction
2. amiotomy
3. cessarian section
- indicated in active stage measured for at least 4 hours without progress
- point of maternal exhaustion
4. forcepts or vaccume options
ectopic pregnancy
what is this? where does it likel occur?
viable?
4 sxs
2 dx
2 tx
pregnancy that implants outside of the uterus 95% occur in the fallopian tube
ALWAYS NON VIABLE
needs immediate attention because is life threatening
SXS
light bleeding
nausea and vomiting
dizziness
abdominal plain
DX:
slow raising HCG (less than doubling every 48 hrs)
US
TX:
- methotrexate
- laproscopic surgery
what are the four most common RF for ectopic pregnancy?
- recent IUD
- hx PID
- interfility txs
- hx of previous ectopic
RH incompatability
what appens in this?
2 tings it can cause in baby?
what does it attack?
2 tests?
tx option?
when the mother is Rh negative and the baby is Rh positive the mothers immune system can attach the baby, typically an issue in second pregnancy when IgG passes through the placenta and enters the + baby causeing in second child hemoyltic anemia and fetal hydrops (death)
attack rhesus D antigen on baby RBC
DX:
1. KLEIHAUER-BETKE TEST-measures occurence and degree of fetomaternal hemmorage
2. COOMBS test-test for antibodies
TX:
rhogam to destroy anti-fetal-rhesus D antibodies at 28-29 weeks
what are 4 complications of Rh incompatability?
- anemia
- hemolytic disease
- fetal hydrops
- still birth
premature rupture of membrane
what is this?
what are the two types and when do they occure?
when are they expected to give birht ?
at risk for?2
Dx 2?
tx
premature rupture of membrane PROM: rupture of the amniotic membrane before the onset of labor at or beyond 37 week gestation
if less than 37 weeks called preterm premature rupture of membranes PPROM
90% of women with PROM will begin labor within 48 hours
RISK with these:
INFECTION aka endometritis and chorioamnionitis
DX:
- sterile speculum examination
- fern testing
Tx:
- deliver the baby if over 34 weeks!! prevents infection
what is the leading cause of maternal mortality worldwide? percent?
postpartum hemorrhage
6%
postpartum hemmorhage
what is this?
2 qualifications?
3 tx options? first line?
blood loss requiring transfusion between admission and the postpartum period
estimated loss:
vaginal: over 500
c-section: over 1000
TX:
- compression
- blood
- oxytocin first line tx!!
just 11 RF for postpartum hemmorhage?
placental issues
baby over 4500 gm
grand multiparity
prolonged labor
medications
obesity
induction
precipitous birth
first baby
instrumental delivery
general anesthesia
uterine rupture
what is this?
fetal mortality?
3 risks?
warning sign?
abnormal thinning of the lower uterine segment
EMERGENCY SITUATION with fetal mortality 50-75%
RISKS:
- high parity
- previous c-section or subsequent long labor
- over stimulation with oxytocin
warning sign: retraction ring across the uterus between symphisis and umbilicus *differentiation of uterine activity during active labor*
placenta previa
what is this?
what should you avoid?
1 sxs?
dx?
2 tx?
when placenta completely/partially covers the OS
DON’T DO VAGINAL EXAMS BECAUSE CAN CAUSE BLEEDING, significant risk of hemmorage
SXS:
- painless bleeding of the vagina hallmark
DX:
US
TX:
- watchful waiting
- cesaran section
multiple gestations
occurence rate of twin, triplet?
why happens more?
best birthing position?
2 MC birth complications?
4 complications for fetus?
twins: 1 in 100
triplets: 1 in 1000
**increased frequency from advanced reproductive technologies**
vertex/vertex allows for vaginal birth
most common complications:
- preterm birth
- spontaneous abortion
complications with twins:
- intrauterine growth restriction
- cord acidents
- death of one twin
- placental previa/ abruptio
preclampsia
what is this a disease of?
2 requirements?
when do you tx?
4 sxs?
1 dx?
2 tx options?
**disease of placental vasculature**
preeclampsia requirements:
1. over 140/90 on 2 occasions 4 hours apart of over 160/110 AFTER 20 weeks gestation in previous normotensive woman PLUS
2. proteinuria over 0.3 gm in 24 hr urine
don’t routinely tx unless BP unless:
SBP over 150
DBP over 100
SXS
- severe headache
- chest discomfort
- SOB
- confusion
DX:
24 hour urine!!!
tx:
labetalol or hydralazine
what is HELLP syndrome?
preeclampsia with
- H-hemoysis
- E-elevated L-iver enzymes
- Low platelets
this is a complication
eclampsia
what is this?
2 tx options
3
1
severe preeclampia with the addition of seizures after 20 weeks gestation
leading cause of maternal and infant illness and death
TX:
1. magnesium sulfate
tx for seizures
neuroprotection for fetus
can prolong pregancy up to 48 hours
2. PREFERRED TX IS DELIVERY!!!
chronic HTN
what is this classified by?
when does this occur?
when to watch?
5 tx for baseline?
2 tx options?
SBP: over 140
DBP: over 90
**occurs prior to pregnancy** and is present BEFORE 20 weeks gestation or persists longer than 12 weeks postpartum
if less than 150/100 WATCH
dx:
get baseline
- 24 hr urine
- UR
- LEFT
- thyroid
- EKG
tx:
- methyldopa
- labetalol
what are 5 complications that can occur from chronic HTN?
- preterm birth
- c-section
- superimposed preeclampsia
- low birth weight
- perinatal death
what percent of women with chronic HTN will have preterm birth? when?
2/3 have preterm delivery
usually at 36-37 weeks instead of 38-40 weeks
preeclampsia superimposed on chronic HTN
what is this?
2 labs?
what percent of women get this?
when a woman with chronic HTN develops proteinuria after 20 weeks gestation
elevated liver enzymes
low platelets
25% of women with chronic HTN will get preeclampsia
gestational HTN
what is this?
when does it occur?
2 PE
2 dx?
HTN DETECTED after 20 weeks gestation without proteinuria
PE
increased BP
no proteinuria
TX:
labetalol
methlydopa
gestational trophoblastic disease
what is this?
what type is most common and of this what are the two types?
what happens in each?
1
2
which one is more common?
spectrum of diseases that arise fom the placenta and include:
- hydatidiform moles (molar pregnancy)-MC and benign
- trophoblastic tumors
- choriocarcinomas
two types of molar preg:
- partial mole
a. egg is fertilized by 1-2 sperm which redulicates itself
b. fetus developes but is NONVIABLE and the placent develops into mass of cysts
- complete mole-MC!!!
grape like vessicles or snowstorm pattern
a. 1-2 sperm combine with egg that has no DNA
b. 20% can develope into malignant tumor (choriocarcinoma)
gestational trophoblastic disease
4 sxs?
2 dx?
2 tx?
SXS:
- abnormal vaginal bleeding
- larger uterine sizes
- hyperemesis gravidum (excessive vomiting)
- preeclampsia
DX:
US
HCG, persistently elevated
TX:
- CHEMOTHERAPY
- SURGERY
gestation diabetes
what is this?
what percent?
target fasting? postprandial?
how to dx?
glucose intolderance that begins or is recognized in pregnancy
gestational diabetes MC in pregnancy (opposed to pregestational Diabetes)-90% gestational!
target range: 90 fasting, 120 post prandial
DX:
- glucose on all pregnany women during first prenatal visit
2. repeat screening at 24-28 weeks
gestational diabetes
explain the pathophys of why this occurs?
- levels of diabetogenic placental steroid and peptic hormones rise linearly through 2nd and 3rd trimester
- lead to increase of glucose levels in blood
3. progressive increase in tissue resistance to maternal insulin, body dose this intentionally because if the mothers tissues are resistant to insulin, she won’t take up the glucose and it will pass through the placenta to nourish the baby, mechanism to make sure the fetus gets nuitrients
3. resistance leads to increase of insulin levels which doesn’t help because the tissues are resistant
4. insulin contributes to post prandial hyperglycemia since it isn’t functioning and can’t take up the sugar!!
5. when post prandial maternal glucose levels rise excessively it causes fetal hyperglycemia** (since it has all passed through placent to fetus) **and fetal hyperinsulinemia (since increases production to deal with massive glucose infux)
6.hyper insulinemia promotes storage excess (since the amount avalible from mom is almost never ending compared to volume of blood avaliable in baby)
7. increased nuitrients lead to macrosomia in baby (enlargement and delayed pulmonary maturation)
how/when do you screen for gestational diabetes? what are the results?
2 times
1.screen 24-28 weeks via two step dx approach of 1 hour screen 135-140 AND 2 abnormal values on 3 hour oral glucose tolerance test that includes 1 of 2 fasting value
- same screening at 6 weeks postpartum!!
**if after being administred the glucose, if elevated, then you know she has DM because she is insulin resistant and it couldnt be taken up in the tissues**
when talking about gestational diabetes what do you need to keep in mind about these populations;
hispanic,
native american,
african, s
outh east asian,
pacific islander,
indigenous australia
BMI over 30,
first degree relative,
hx of GDM in pas
need to screen earlier because they are like to devlope disease sooner
what are the tx options for gestational diabetes?
1. glyburide or insulin in uncontrolled diabetes with diet modification/exercise
- ADA diet
if mother is on insulin and other meds for gestational diabetes…when do you want themto deliver? what should you offer?
39 weeks, might need induction
offer c-section if weight over 4500
what are mothers with gestational diabetes at increased risk for?
T2DM in 5-10 years so screen annually
10-50% risk
what is the chance of spontaneous abortion if less than 20 weeks gestation?
20%
aka
1:5
important to let mothers know this is common!
when is HCG first detected? doubling time?
first detected 11 days after conception
48 hour doubling time!
what are 5 additionaly considerations to be mindful of in a new mom who is going to be going through the birhting process?
2
- thyroid function-test
- maternal infection
a. HERPES-always inspect before labor
b. group B
culuture at 36 weeks since transient on skin and can cause major problems, if pos tx with Peniciilin G
- obesity
- asthma
control can change during pregnancy by 1/3s so just be concious
- UTI
prolonged rupture of membranes
risk?
tx?
risk of infectioun
tx:
ampicillin and gentamycin
if fever add clindamycin
pelvic inflammatory disease
what is this? 2 ways to get it?
5 RF!
4 sxs, 1 buzz word
3 dx
1 tx
polymicrobial infection of the upper reproductive tract (uterus, fallopian tubes, and ovaries) that can be either from sexually transmitted or exogenous bacterial
**the bacteria ascent!**
RF:
1. younger than 25
2. nonbarrier contrception
3. hx of new or symptomatic sex partners
4. previous PID
5. STI
SXS
1. lower abdominal/back pain
2. fever
3. esquisitly tender cervix on bimanual exam
chandelier sign!
4. purluent discharge
DX:
- test for gonnorhea/chlamydia (since most common)
- transvaginal US
- diagnostic laproscopy may be needed
TX:
ABX!!!!
what are the four most common cause of PID?
- gonnoreah
- chlamydia
- staph
- strep
metritis
what is this?
inflammation of the wall of the uterus
