Gynecology Flashcards
precocious puberty- age cut-off
before age 8 in girls
before age 9 in boys
does not always have to be treated if not serious or impactful
precocious puberty causes
familial/genetic (nonpathologic)
central (True) precosious puberty: early activation of hypothalamic pituitary- gonadal axis
- image the head
- continuous GnRH analog will suppress LH and FSH
pseudoprecocios puberty: autonomous excess secretion of sex steroids
- image the abdomen
- surgical tumor removal
congenital adrenal hyperplasia
-cortisol replacement
complications:
short stature
social and emotional adjustment issues
precocious puberty isosexual vs heterosexual
iso: premature sexual development appropriate for gender
10% due to CNS lesions/trauma
Complete- all sexual characteristics develop prematurely
incomplete- only 1 sexual characteristic develops prematurely
hetero: virilization of girls (exogenous androgens, androgen- secreting neoplasm, congenital adrenal hyperplasia)
feminization of boys
precocious puberty isosexual vs heterosexual
iso: premature sexual development appropriate for gender
10% due to CNS lesions/trauma
Complete- all sexual characteristics develop prematurely
incomplete- only 1 sexual characteristic develops prematurely
hetero: virilization of girls (exogenous androgens, androgen- secreting neoplasm, congenital adrenal hyperplasia)
feminization of boys
precocious puberty causes
familial/genetic (nonpathologic)
central (True) precosious puberty: early activation of hypothalamic pituitary- gonadal axis
pseudoprecocios puberty: autonomous excess secretion of sex steroids
precocious puberty isosexual vs heterosexual
iso: premature sexual development appropriate for gender
10% due to CNS lesions/trauma
Complete- all sexual characteristics develop prematurely
incomplete- only 1 sexual characteristic develops prematurely
hetero: virilization of girls (exogenous androgens, androgen- secreting neoplasm, congenital adrenal hyperplasia)
feminization of boys
pregesterone
pro-gestation stimulates endometrial development inhibits uterine contraction increases thickness of cervical mucus increases basal body temp inhibits LH and FSH secretion
decrease in progesterone level leads to menstruation (simulate this by giving progesterone and then stopping it)
bHCG
maintains corpus luteum and progesterone secretion
mean age of menarch in the US
13
pregesterone
pro-gestation
True precocious puberty
high LH and FSH
GnRH will increase FSH further
treat by inducing menopause with continuous GnRH analog
mean age of menarch in the US
13
Pseudoprecocios puberty
low LH and FSH
no response when GnRH given
True precocious puberty
high LH and FSH
GnRH will increase FSH further
how long is luteal phase
13-14 days
FSH triggers release of which hormone from follicle?
estradiol
Menopause
end of menstruation due to cessation of ovarian function
Average age: 51.5 years
Premature ovarian failure: amenorrhea for at least 1 year before age 40
Labs, which are not so necessary would show
increased FSH, LH,
decreased estrogen
Menopause is diagnosed with 12 months of amenorrhea in a woman over 45yo (diagnostic and requires no additional work-up)
A woman over age 45 with irregular menses (oligoamenorrhea) and menopausal symptoms (hot flashes, mood changes, sleep disturbances) can be assumed to be going through perimenopause
Serum FSH increases in the perimenopausal period and after menopause, but this is of little diagnostic value beyong obtaining a menstrual history and history of symptoms
If younger than 45, other etiologies for oligo/amenorrhea must be excluded (TSH, serum hCG, prolactin, FSH)
Premature ovarian failure:
amenorrhea for at least 1 year before age 40, or high FSH + menstrual irregularity before age 40
tobacco radiation chemo abdominal disorders pelvic surgery
Perimenopause
ovarian response to FSH and LH decreases
FSH and LH levels increase
Estrogen levels fluctuate
irregular bleeding, sometimes heavier flow
Endometrial biopsy to r/o other causes
Menopause symptoms
hot flashes breast pain sweating fatigue anxiety/depression dyspareunia urinary frequency and dysuria changes in bowel habits vaginal atrophy bladder symptoms stress urinary incontinence
Menopause treatment
Women’s Health Initiative- gave asx post- menopausal women estrogen and progesterone to see if it is cardioprotective, and they had more heart attacks and cardiac events so estrogen is now only used to treat symptoms
Topical estrogen is contraindicated in anyone with history of estrogen- sensitive or breast cancer
Dyspareunia can be treated with
- lubricating agents
- vaginal estrogens
Osteoporosis:
- calcium
- vitamin D
- weight-bearing exercise
- bisphosphonates
- selective estrogen receptor modulators (SERMs)
Hot flashes and mood swings:
-hormone replacement therapy at least for a little while
Pros and cons of hormone replacement therapy for menopause
Pro:
- control of menopause symptoms (hot flashes, vaginal dryness/atrophy, urinary incontinence, emotional lability
- reduced risk of osteoporosis
- reduced risk of colorectal cancer
CONS
- not indicated for prevention of chronic disease, stroke, heart disease, and osteoporosis (USPSTF)
- HRT doubles risk of
- invasive breast cancer (+8 per 10,000) but not noninvasive breast cancer
- endometrial cancer
- venous thromboembolism (+8 PEs per 10,000)
- increases risk of stroke by up to 32-41% (+8 per 10,000)
- increases risk of heart disease by 29% (+7 per 10,000)
- However, if taken at ages 50-59, HRT results in less coronary calcifications on CT scan. This may or may not correlate with less risk of heart disease in women taking HRT during ages 50-59.
- increases risk of biliary disease and need for biliary surgery
Non-hormonal options for treating hot flashes
- Venlafaxine- a good choice if any depression, anxiety, fatigue, isolation. Good first- line drug
- Desvenlafaxine: only non-hormonal drug that is FDA-approved for hot flashes. Also works as an antidepressant
- Clonidine- a good choice if BP control is also needed. SE- dry mouth, constipation, drowsiness
- Gapabentin- good choice if insomnia, restless leg syndrome, seizure d/o, neuropathy, chronic pain
- Time- about 30-50% of women have symptoms improvement within a few months, and most have resolution within 4-5 years
- Placebo: placebo effect is about 20-25% effective in reducing hot flashes
Side effects of estrogen therapy
weight gain nausea breast tenderness headache endometrial proliferation
Side effects of progesterone therapy
acne
depression
hypertension
Primary Amenorrhea
16yo with normal secondary sex characteristics but no menses
13yo with absence of both menses and secondary sex characteristics
Causes of primary amenorrhea
hypothalamic or pituitary dysfunction
anatomic abnormalities
- absent uterus
- vaginal septum
- imperforate hymen
chromosomal abnormalities with gonadal dysgenesis
-Turner syndrome (45XO)
Secondary amenorrhea
absence of menses >6 months in a patient with a prior history of menses
causes: pregnancy premature ovarian failure hypothalamic or pituitary disease acquired uterine abnormalities polycystic ovarian syndrome hyperprolactinemia thyroid disease anorexia nervosa or over-eating
Asherman syndrome
scarring of the uterus that follows infection or postpartum procedure
H and P menstrual history family history medications signs of masculinization -facial hair -voice deepening Tanner stages
Labs to check in amenorrhea
1. beta HCG Thyroid studies (TSH and free T4) Prolactin FSH and LH Androgens -testosterone and DHEA
- progesterone challenge
estrogen-progesterone challenge
progesterone challenge
is the woman producing estrogen and/or having ovulatory cycles?
estrogen stimulates growth of endometrial lining
If a woman doesn’t ovulate then there isn’t a release of progesterone that stabilizes what has grown
After stopping progesterone, there should be menstruation, but only if estrogen was normal and built up the endometrial lining
If progesterone challenge lead to bleeding, consider anovulation to be the explanation for amenorrhea
if progresterone challenge has no effect, then suspect low estrogen levels or outflow tract obstruction to be the causes of amenorrhea
- estrogen-progesterone challenge
estrogen-progesterone challenge
Give estrogen to ensure that the endometrial lining can be present
If the withdrawal of these hormones induces menstruation then you know the patient has a normal outflow tract
What are the basics of a workup of primary amenorrhea
- congenital defects: imperforate hymen, transverse vaginal septum, vaginal agenesis
- if signs of hyperandrogenism, serum testosterone and DHEAS to assess for androgen- secting tumor
- if galactorrhea, then serum prolactin and thyrotropin to assess for prolactinoma
If physical exam shows possible absence of uterus, then obtain a pelvic sonogram
- if uterus absent, then check karyotype and serum testosterone
- androgen insensitivity syndrome (46,XY; elevated testosterone)
- abnormal mullerian development (46, XX; normal female testosterone levels) - If the uterus is present, check beta-HCG and FSH
- if beta-HCG is high- pregnancy
- if FSH low -cranial MRI for hypothalamic or pituitary diseas
- if FSH normal- serum prolactin and thyrotropin
Labs to order for secondary amenorrhea
- serum bHCG to rule out pregnancy
- thorough H and P
- serum prolactin (rule out hyperprolactinemia), serum TSH (rule out thyroid disease), serusm FSH (rule out ovarian failure)
- If signs of hyperandrogenism, then serum DHEAS and total tetosterone
- If all the above are normal or history of dilatation and curettage (D and C), abortion, miscarriage, then progestin withdrawal test (rule out Asherman syndrome)
Treatment for amenorrhea
- modify behavior
- surgical correction
- GnRH or gonadotropin replacement- Leuprolide
- Dopamine agonists
- hormone replacement therapy for symptom management
- Lysis of adhesions and estrogen administration if Asherman syndrome
Primary dysmenorrhea
inflammation/trauma of shedding of endometrial lining
crampy lower abdominal pain n/v HA diarrhea mild tenderness
Secondary dysmenorrhea
Endometriosis PID Fibroids Cysts Adenomyosis
Risk factors for dysmenorrhea
menorrhagia
menarche
dysmenorrhea workup
rule out pregnancy cervical or vaginal cultures urinalysis NSAIDs (less pain and less bleeding if initiated the day before bleeding and continued 16hrs throughout bleeding) hormonal contraception
premenstrual dysphoric disorder (PMDD) and PMS
pain
abnormal mood
autonomic symptoms
in the luteal phase
interferes with daily life characterized by weight gain HA abdominal/pelvic pain abdominal bloating change in bowel habits food cravings mood lability depression fatigue irritability breast tenderness edema abdominal tenderness acne
RF: family history
Tx: NSAIDs, hormonal contraception, exercise, B6, progesterones, SSRIs just during symptoms (5 days per month)
Endometriosis
endometrial tissue outside of the uterus
ovaries broad ligament bowel bladder lungs brain
Theories: retrograde menstruation vascular spread lymphatic spread iatrogenic spread metaplasia
RF:
nulliparity
family history
infertility (50% of cases)
clinical features;
- pelvic pain (most severe during menses, 2-7 days prior to menses and possibly at ovulation)
- 3Ds: dysmenorrhea, deep dyspareunia, and dyschezia (painful defecation during menses), possible blood in stools during menstruation
- infertility
Physical findings:
- localized tenderness in the cul-de-sac or oterosacral ligaments (especially at the time of menses)
- palpable, tender nodules in the cul-de-sac, uterosacral ligaments or rectovaginal septum
- pain with uterine movement
- tender, enlarged adnexal masses especially if there are endometriomas
- Adhesions causing a fixed or retroverted uterus
Labs:
CA-125 increases, not very meaningful though
Biopsy:gunpowder, chocolate
Treatment:
expectant management
pain control with NSAIDs
hormonal therapies: combined OCPs dosed continuously
GnRH agonist given continuously for 6-12 months
Progestin
Danazol
Aromatase inhibitors stop conversion of androgens to estrogens, to decrease stimulation to endometrium
Surgical intervention
laparoscopic surgery
lysing adhesions, addressing infertility, and collecting biopsy specimens in doing so
hysterectomy with bilateral salpingo-oophorectomy (take the ovaries, which secrete much hormone), then proceed with hormone replacement
Adenomyosis
growth of endometrial tissue within uterine wall
painful
The 3 Ds of endometriosis
dysmenorrhea
deep dyspareunia
dyschezia
Common causes of abnormal uterine bleeding
fibroids cancer HPO dysfunction clotting disorders-von Willebrand disease Threatened abortion Molar pregnancy Ectopic pregnancy
PALM-COEIN causes of abnormal uterine bleeding
PALM-COEIN polyp adenomyomas leiomyoma malignancy and hyperplasia coagulopathy ovulatory dysfunction endometrial iatrogenic not yet classified
Workup for abnormal uterine bleeding
H an P:
Ask about the menstrual cycle: how long is it usually?
is it heavy? is it related to intercourse? associated symptoms? family history of bleeding disorder bleeding with medical procedures? contraceptive history rule out GI bleeding and bleeding from the urinary tract
A change in the menstrual cycle clues us into abnormal pathology
Labs: pregnancy test CBC homrones: testosterone, TSH, FSH, LH, prolactin coagulation studies
pap smear
STD testing
endometrial biopsy if >45yo
or if
How long is a menstrual cycle, typically?
21-35 days
polymenorrhea
oligomenorrhea
menstrual cycle >35 days
How long does the period usually last, and how much blood loss is normal?
Generally 3 hrs
seldomly needs to change pads during the night, only passes clots
menorrhagia
Excessive bleeding
Metrorhagia
frequent bleeding
irregular periods- causes
ovulatory dysfunction
anovulatory bleeding is typically heavy, as it occurs only when blood supply to an overgrown endometrium becomes insufficient
regular heavy bleeding suggests fibroid, adenomyosis, or polyp
Bleeding related to intercourse
cervical lesion or polyp
glandular tissue on cervix
MCC AUB
ovulatory dysfunction
AUB and positive bHCG, + intrauterine pregnancy and closed os
threatened abortion
AUB and enlarged uterus + menoetrorrhagia for months
fibroids, molar pregnancy, adenomyosis
AUB and bleeding associated with severe menstrual pelvic pain
endometriosis, adenomyosis
AUB and menorrhagia in a perimenopausal woman
endometrial cancer or hyperplasia
AUB started with menarche
coagulopathy, vWF
AUB and positive bHCG+ severe pain + no fetus in uterus on US
ectopic pregnancy
AUB and metrorrhagia especially after intercourse + no pain + normal-sized uterus
polyp or glandular tissue on cervix
AUB and depression and constipation and abnormal uterine bleeding
hypothyroidism
How do we treat AUB?
MCC is anovulatory cycle, in which case OCP is helpful
NSAIDs reduce uterine bleeding by reducing prostaglandin synthesis in the endometrium, leading to vasoconstriction
Endometrial ablation
Hysterectomy
Otherwise, treat the underlying cause
Admit if hemodynamically unstable
-IVF, blood transfusion, intrauterine tamponade, uterine curettage (hyperplasia, neoplasia?), IV high-dose estrogen + antiemetic which will stabilize the lining of the endometrium, uterine artery embolization, hysterectomy
indications for endometrial biopsy
over 45yo
multiple risk factors for endometrial cancer
persistent abnormal uterine bleeding > 6 months
PCOS- pathophysiology and diagnosis
MCC androgen excess in women
MCC amenorrhea from a pathologic standpoint
overproduction of LH increased androgen produced in both ovaries and adrenals, increased estrogen in the periphery... leading to -amenorrhea -infertility -DM -hirsutism
increased ovarian androgen production through estrogen
diagnosis: 2 of these 3 things:
1. anovulation or oligoovulation (amenorrhea or oligomenorrhea)
2. androgen excess
3. polycystic ovaries on US
Excess LH stimulates the theca cells of the ovaries to produce androgens
Some of the androgens are converted to estrogens by aromatase enzymes in adipose cells in the periphery
Increased LH secretion
Insulin also stimulates androgen production and inhibits sex hormone binding globulin (increased proportion of free hormone)
PCOS H and P
obesity hirsutism acne, male pattern hair loss voice deepening clitoromegaly menstrual dysfunction infertility ovarian enlargement that is mild to moderate- lots of small to moderate-sized follicles resulting from the disease, prevents formation of a normal dominant follicle so that ovulation is abnormal Labs: increased LH LH:FSH>2:1 increased androgens: testosterone, DHEA, androstenedione
positive progestin challenge, proving that the patient is not ovulating
Radiology
multiple small to medium sized follicles on the periphery of the ovary- string of pearls
PCOS treatment and treatment
Give progesterone to protect the uterus from cancerous change
Exercise and weightloss
Combined OCPs
Progesterone
Metformin (weightloss, improved BP, cholesterol, may assist with infertility)
Spironolactone to decrease anti-androgen effects
Statin
Clomiphene can induce ovulation
Antibiotics or dermatologic creams
Complications:
infertility
diabetes
increased risk of endometrial cancer (inadequate progesterone)
Pelvic prolapse
fascial defects
H and P: pelvic pressure/heaviness feeling that something is falling out of the vagina "I'm sitting on an egg" urinary/fecal incontinence dyspareunia
Risk factors: age pregnancy vaginal delivery increased abdominal pressure -obesity -chronic cough -lifting -constipation
treatment:
pelvic floor exercises
pessary (space-occupying device)
surgery
lab findings consistent with PCOS
increased LH (LH:FSH ratio > 2:1)
increased testosterone
increased DHEA
increased androstenedione
When can lactation be an effective form of contraception
if
Vaginitis- what are the 3 main types?
bacterial vaginosis
trichomoniasis
fungal vaginitis
bacterial vaginosis
imbalance of vaginal flora
lactobaccili usually dominate
they decrease in concentration while Garnerella vaginalis becomes more prevalent
thin, white, gray discharge with fishy odor
vaginal pH>4.5
wet mount- clue cells
clue cells are epithelial cells covered in coccobacilli
Whiff amine test: fishy odor emitted with 10% HCL is dropeed onto the vaginal discharge
Treatment: metronidazole for 7 days
Trichomonas vaginalis
thick, frothy, green discharge
“strawberry cervix”
motile trichomonads on wet mount
treatment- metronidazole (one large dose of metronidazole 2g)
Both sex partners should be treated
Vaginitis- candida
RF: antibiotic use increased estrogen level DM immunosuppression
Diagnosis:
Vaginal itching/irritation
budding years and pseudohyphae on wet mount
Treatment:
oral fluconazole
topical azole
Toxic shock syndrome
prolonged tampon use
classic presentation: hypotension fever rash involving palms/soles sore throat HA myalgia GI symptoms
Dx:
culture staph aureus from the vagina
Tx:
remove tampon
clindamycin (decreases toxin production)
vancomycin (covers MRSA until the strain is known)
Cervicitis: G and C infection at columnar epithelial cells
Both G and C cause PID by breaking the cervical mucosal barrier, and ascending into the peritoneal cavity
Asymptomatic: annual screening for all sexually active females
PID
linked to GC infection untreated other pathogens: bacteroides e. coli streptococci
tubo-ovarian abscess
ectopic pregnancy
chronic pelvic pain
infertility
symptoms may be worse just after menstrual period, when the cervical barrier is broken for a short time
pe: cervical motion tenderness -Chandelier sign uterine tenderness lower abdominal tenderness -RUQ tenderness, Fitz Hugh Curtis syndrome
DX:
nucleic acid test for G/C
Labs: pregnancy test WBC ESR nucleic acid amplification tests -gonorrhea -chlamydia
gram stain and culture
culdocentesis- stain and culture purulent fluid
radiology:
transvaginal ultrasound can be used to detect an abscess
risk factors:
multiple sex partners
15-25yo age range
barrier contraceptions provides some protection
Treatment:
polymicrobial-
streptococci, gram neg cocci, anaerobes, g/c coverage
determine if inpatient or outpatient
if high fever, unstable VS, unreliable, keep patient inpatient
IV therapy example: Cefotatan+doxycycline or Cefoxitin+doxycycline or Clindamycin + gentamicin
outpatient therapy example:
ceftriazone
doxycycline
metronidazole
cefotaxime, cefoxitin + probenecid
Syphilis
treponema pallidum
STD
perinatal infection also possible
primary:
- papule
- painless, clean base
- heals spontaneously
secondary:
- fever, malaise, lymphadenopathy, RASH
- mucous patches in the mouth, grey condyloma lata
- early and late phase
early latent or late latent phase:
asx
tertiary: end stage, 1-25 years after initial infection
CNS:general paresis, tabes dorsalis, pain, Argyll Robertson pupil
CV:aneurysm of ascending aorta
skin
gummas: granulomatous lesions in skin, bones, internal organs
Diagnosis: Nontreponemal tests- RPR VDRL Confirm with treponemal tests for antibodies against treponemes or direct observation of syphilis
Treatment:
Penicillin G IM x1 for every primary, early, latent
Penicillin G IM qweek x3 Late syphilis
Penicillin G IV for neurosyphilis
if allergic to PCN G, then tetracycline or doxycycline
Follow treatment with RPR titer
Argyll-Robertson pupil
will constrict on accomodation but not on direct light
Genital herpes
HSV2
first outbreak is largest, with recurrences smaller, painful, usually in the same place
HPV warts
types 6 and 11: genital warts treatment: -cryotherapy -lazer therapy -podophyllin -imiquimod -topical 5-fluorouracil -alpha-interferon injection -excision
remains latent in tissues and can recur
HPV cervical cancer
16 and 18: cervical cancer
penile, anal, head and neck cancer
Pap smear
Chancroid
rare in the US haemophilus ducreyi painful ulcer purulent ulcer enlarged lymph nodes that drain pus
gram stain of exudate shows GNR
treatment:
ceftriazone
azithromycin
Lymphogranuloma venerium
L1, L2, L3 serovars of chlamydia trachomatis
causes a papule at site of inoculation that ulcerates, Painless, resolves spontaneously
U/L lymphadenopathy that leads to buboe formation
If acquired via anal sex, a bad proctocolitis can result!
serology, nucleic acid therapy
treatment:
doxycycline
complications: fistulas and strictures
Granuloma inguinale
Klebsiella granulomatis
rare in the US
beefy red painless ulcers that gradually progress
no inguinal lymphadenopathy
Donovan bods on wright-giemsa stain (they look like rods in the cell)
Treatment:
Doxycycline
Vaginosis versus trichomonas versus candida
whitish gray fishy discharge, clue cells, high pH (>4.5)
trich has thick, frothy greenish discharge, motile trichomonads, high pH (>4.5)
candida has pseudohyphae on wet mount, with pH 3.5-4.5
Treatment: Gonorrhea
Ceftriaxone
Treatment: chlamydia
Doxycycline, azythromycin
Culture negative cystitis
suspect chlamydia
Anticholinesterases, organophosphates
atropine, pralidoxime
Abnormal uterine bleeding
beta HCG Pap wet prep GC probe CBC bleeding time PT/INR PTT TSH Endometrial biopsy
uterine fibroids
benign tumors composed of smooth muscle
each one is monoclonal
stable and steady, then shrink after menopause as hormone levels drop
RF: family history ethnicity black>white 70-80% incidence nulliparity obesity PCOS
H and P: asymptomatic menorrhagia dysmenorrhea pelvic pain/pressure infertility enlarged uterus with irregular contours
Radiology:
transvaginal ultrasound
hysteroscopy
MRI
If symptomatic, then treat
Treatment for menorrhagia: Continuous GnRH agonists -leuprolide hormonal contraception myomectomy to preserve fertility hysterectomy if patient is symptomatic uterine artery embolization (high rate of ovarian failure and impaired fertility after this, so only do this in women who are done with child-bearing)
Endometrial cancer
Adenocarcinoma of uterine glands
commonly caused by exposures to high estrogens or unopposed estrogens
aka estrogens without progesterone
Type 1: 85%
estrogen- responsive
Type 2: 15%
not related to excess estrogen
worse prognosis
RF: unopposed estrogen 2/2: PCOS Obesity HRT nulliparity
DM
HTN
age
FHx of Lynch syndrome (HNPCC)
H and P: Abnormal bleeding -heavier or longer periods -bleeding between periods -postmenopausal bleeding
Labs/testing:
atrophic vaginitis is common, but endometrial biopsy anyway to r/o cancer
embx:
1. >35 and heavy menses
2. postmenopausal bleeding
hysteroscopy
CA-125 (better just for monitoring response to therapy)
Radiology:
ultrasound
CT
Treatment: total abd hysterectomy with bilateral salpingo-oophorectomy lymph node sampling/dissection debulking chemotherapy radiation hormonal therapy
Complications:
loss of organs
metastasis
prognosis is great if the cancer is caught early
96% 5 year survival if caught early
Cervical cancer
squamous cell cancer (pap), exterior
adenocarcinoma (endocervical)
Pap at the transitional zone
progression from normal to mild dysplasia (CIN 1) to moderate dysplasia (CIN 2) to severe dysplasia (CIN 3) to in situe carcinoma (CIN 3) to invasive carcinoma
RF:
HPV
Types 16 and 18 make up 70% of cervical cancers
Early 1st intercourse multiple sexual partners history of STDs immunosuppression tobacco use (decreases immune system)
Pap smear age
initiate at 21yo
screen every 3 years for ages 21-29
patients 30+ may continue pap smear every 3 years, or may opt for Pap smear and HPV testing every 5 years (preferred by some professional organizations)
Screen more frequently in women who are in high risk groups
stop as early as age 65 if adequate normal Pap tests
if hysterectomy for benign disease, there is no need to screen for cervical cancer
Bethesda classification of cervical dysplasia
SU 11-6
Atypical squamous cells of undetermined significance (ASCUS)
false positive?
early dysplasia?
high grade changes?
repeat the test in one year if 21-24 yo
if older than 25yo, test for HPV
If the pap or HPV are positive, proceed to colposcopy, which allows you to do a directed biopsy
Atypical squamous cells cannot exclude HSIL (ASC-H)
colposcopy
Atypical glandular cells of undetermined significance (AGUS)
here we worry about adenocarcinoma, which arises high in the endocervical canal/ uterus/ fallopian tubes
Endocervical sampling Colposcopy Endometrial biopsy (>35 years old or risk factors)
Follow this patient very closely
Low grade squamous intraepithelail lesions (LSIL)
This should correspond to CIN
low chance of conversion to cancer
Age:
21-24 yo: repeat pap in 1 year
25-29yo: colposcopy
> 30yo: HPV test (if positive then colpo, if negative then repeat Pap and HPV test in 1 year)
High grade squamous intraepithelial lesion
CIN 2 or 3
HSIL
Age?
21-24 yo: colposcopy
>25yo: Loope electrosurgical excision procedure (LEEP)
people with positive pap later in life are not as good at fighting off the virus and are therefore at higher risk of cancerous change
LEEP if patient is done having kids or if you are afraid of losing the patient to follow up
If CIN2 or 3 on colpo, then LEEP. If high grade findings persist, low threshold for removing tissue
cervical cancer H and P, ppx, excision, radiology
H and P: asx postcoital bleeding watery discharge symptoms related to lateral compression of lymphatics, veins, ureters
Pap test
Colposcopy
Excision procedures:
- LEEP
- Cold knife conization
Radiology
CT or MRI to look for spread
IVP to look for compression of the ureters
Treatment: Microscopic invasion: -simple hysterectomy -conization -lazer ablation
Gross invasion:
-radical hysterectomy and lymphadenectomy
Extension and metastasis:
-chemo and radiation
Indications for EMBX
Age >35
- menometrorrhagia
- postmenopausal bleeding
Age
varicocele that does not empty when the patient is recumbent
renal cell carcinoma
3 meds often used to treat ileus
erythromycin
neostigmine
metoclopramide
Treatment for squamous cell cancer of the vagina
stage 1 (2cm): external beam radiation
Stage 2, 3, 4: external beam radiation +/- adjuvant therapy
(RADIATION)
Lichen sclerosis
benign chronic inflammatory condition of the anogenital region, most commonly affecting postmenopausal women
vulvar pruritis and pain
PE: thinning skin with ivory white or porcelein white plaques and macules
Treatment: low threshold for punch biopsy to rule out SCCl steroids (clobetasol) or pimecrolimus, steroids
Benign ovarian tumors
physiologic aka functional cysts
- follicular cysts
- corpus luteum cysts
arising from normal menstrual cycle
If the follicle doesn’t rupture on ovulation then you get a follicular cyst
If the corpus luteum is supposed to involute but it doesn’t then you end up with a corpus luteum cyst
frequently asymptomatic, sometimes abd discomfort
acute pain in the setting of rupture or torsion
increased CA-125, though this is non-specific
US: benign findings (cystic, smooth edges, few septa)
malignant findings: irregularity or nodularity, multiple septa, extension or adhesions
Treatment: observation, may go away on it’s own
- cystectomy unless there are malignant characteristics on ultrasound
- oophorectomy
- TAH-BSO
Complications:
ovarian torsion
Mucinous or serous cystadenoma
epithelial tumors psammoma bodies can grow very large sometimes bilateral usually asymptomatic until very big not cancerous in general
Surgical excision allows confirmation of diagnosis, with reduced risk of ovarian torsion
Endometrioma
seen with endometriosis
walled off collection of endometrial tissue in ovary
can bleed or shed in a monthly cycle; the blood doesn’t have anywhere to go because it is walled off, so the endometrioma continues to enlarge and cause pain and scarring
can be painful or asx
if very large, doesn’t regress on it’s own and pt then benefits from surgical removal
(chocolate cyst)
Benign cystic teratoma
"dermoid cyst" benign germ cell tumor contains multiple dermal tissues -endoderm -mesoderm -ectoderm
can contain hair, teeth, sebaceous glands
usually asymptomatic
with a small chance of malignant transformation (1-2%)
Treatment:
cystectomy
sometimes the ovary must be removed as well
Stromal cell tumors
arise from granulosa, theca, or Sertoli-Leydig cells
granulosa and Leydig cells produce estrogen, leading to precocious puberty (granulosa) or virilization (androgen), depending on which cells are involved
Malignant potential is significant
Tx:U/L salpingo-oophorectomy
Ovarian cancer
epithelial (65%) germ cell (25%)
RF: BRCA1 and BRCA2 mutations
Nulliparity
Early menarche
Late menopause
Infertility
H and P:
microscopic and asx in early stages
there is no good screening
advanced cancer presents with abdominal pain, fatigue, weight loss, change in bowel habits, menstrual irregularities, ascites, palpable mass on bimanual exam
Labs: CA-125, which has an especially strong association with epithelial cancer alpha- fetoprotein hCG LDH Estrogen Testosterone
Radiology:
ultrasound
MRI or CT to look for spread
Treatment:
surgical resection
do not biopsy, because the risk of causing spread 2/2 cyst rupture is significant
TAH- BSO
Peritoneal washings
Lymph node dissection
Omentectomy
infinite implants, microscopic
debulking
treat microscopic disease with chemotherapy adjuvant therapy
with germ cell tumors:
u/l salpingo-oophorectomy
surgical debulking and chemotherapy for more extensive disease
prognosis is low because we don’t detect this until late
false positive rate is high for available screenings
psammoma bodies
Serous cystadenocarcinoma
estrogen excess
Granulosa-theca cell tumor
androgen secretion
Sertoli-Leydig cell tumor
diastolic murmur heard best in left lower sternum that increases with inspiration
tricuspid stenosis
late diastolic murmur with an opening snap (no change with inspiration)
mitral stenosis
systolic murmur heard best in the second right interspace
aortic stenosis
systolic murmur heard best in the second left interspace
pulmonic stenosis
Late systolic murmur best heard at the apex
mitral prolapse
diastolic murmur with a widened pulse pressure
aortic regurgitation
holosystolic murmur louder with inspiration at the left lower sternum
tricuspid regurgitation
holosystolic murmur heard at the apex, radiates to the axilla
mitral regurgitation
Gynecomastia
a male breast disorder
causes:
puberty (resolves spontaneously in 6 months to 2 years)
Drugs: "some drugs cause awesome knockers" Spironolactone Digoxin Cimetidine Alcohol Ketoconazole
STACKED Spironolactone THC Alcohol Cimetidine Ketoconazole Estrogen Digoxin
Herbal agents: tea tree oil, lavender oil
Cirrhosis Hypogonadism Testicular germ cell tumor Hyperthyroidism Hemodialysis patients
Breast abscess
might start as mastitis
-staph infection in the milk ducts that occurs during breastfeeding
-walled-off collection of pus= breast abscess
RF: smokers, diabetics
H and P: painful mass on the breast fever (102-103 F) broad area of redness, warmth, tenderness Purulent drainage
US if suspicion of abscess
Treatment: oral or IV abx: dicloxacillin caphalexin Amoxicillin-clavulanic acid TMP-SMX Metronidazole
drain the abscess
pack the wound
continue breast feeding to keep fluid moving (abscess forms because of static milk)
FIbrocystic changes
increase in benign cysts and fibrous tissue
multiple bilateral masses
hormone sensitive
worse before menstruation (re-examine after her period)
breast pain preceding menses
Biopsy: epithelial hyperplasia
US: distinguish between solid mass and large cyst
Treatment:
reduce caffeine or dietary fat
birth control pills can prevent spike in estrogen
Fibroadenoma
most common benign breast tumor especially in women under the age of 30
US:is it mass or cyst?
FNA: mass or cyst?
May not need a mammogram
if 35, more concerned about cancer and you might want a mammogram
surgical excision (symptoms with larger)
cryotherapy
may recurr
intraductal papilloma
benign lesion of ductal dissue
bloody nipple discharge
could be serious
spontaneous discharge is worrisome, especially bloody,
excise papilloma to evaluate the cancer
Phyllodes tumor
large, bulky tumor
more common in women in their 50s
leaflike cleft:generally benign, can become malignant
most common tumor in teen and young women
fibroadenoma
most common mass in patients 25-50
fibrocystic change
presents with serous or bloody nipple discharge
intraductal papilloma
What gene mutation is commonly seen in men with breast cancer?
BRCA2 mutation
breast cancer risk factors
family history genetic mutation estrogen exposure -early menarche -late menopause -nulliparity -late first pregnancy -HRT advanced age obesity alcohol certain chemicals and pesticides
breast cancer presentation
asx until a mass is felt
solid and immobile is worrisome
peau d’orange- lymphedema
new nipple retraction (ductal involvement or suspensory lig)
axillary lymphadenopadhy
upper outer quadrant most commonly affected
types of breast biopsy
FNA: cyst versus solid
solid can’t diff between cis and invasive CA
Core biopsy better for solic mass
open biopsy- use US to locate then remove all around it
Ductal carcinoma in situ (DCIS)
malignancy arising from duct without invasion
precancerous
Treatment:
lumpectomy + possibly radiation
mastectomy if high risk
Lobular carcinoma in situ (LCIS)
malignancy arising from lobule without invation
high likelihood of cancerous change somewhere in the breast, though not necessarily at that site
higher likelihood of breast cancer than with DIS
risk factor for subsequent cancer on the same side AND the contralateral side
Always ER and PR+
Treatment:
observe, overall higher risk of cancer than DCIS
SERMs (tamoxifen or raloxifene)
Excisional biopsy
Prophylactic bilateral mastectomy
drug therapy is helpful because LCIS is ALWAYS ER/PR positive
infiltrating ductal carcinoma
fibrotic response in the surrounding tissue
most common form of invasive breast cancer (80%)
palpable firm fixed mass
Treatment: indications for mastectomy + sentinel node biopsy: -early and focal, + radiation -large (>5cm) + radiation -multifocal
If metastatic disease or large tumor (>1cm) or aggressive tumor: chemotherapy
infiltrating lobular carcinoma
less fibrous than ductal (palpable, firm, fixed)
often multifocal
bilateral
slower growing, slower to metastasize
inflammatory carcinoma (a type of presentation that can apply to many types of breast cancer)
inflammatory carcinoma:
rapidly growing
very poor prognosis
looks like ductal, except that there are inflammatory changes (erythema, warmth, pain)
high level of suspicion, perhaps a patient with recurrent mastitis
Paget disease of the breast
eczema-like patches on the nipple and areola
caused by malignant cells that infiltrate the epidermis
may also indicate underlying cancer in the breast parenchyma
Hormone therapy in breast cancer
Always look for these three receptor types:
estrogen and progesterone
receptors
HER2/Neu: trastuzumab (hereptin) ab against those receptors
BRCA mutation PPX
b/l ppx mastectomies and oophorectomies to reduce risk of breast cancer and ovarian cancer later in life
Breast cancer complications
mets: bone thorax brain liver
lymphedema: wound healing, infection, ROM, pain
most common breast cancer
invasive ductal carcinoma
what findings are suspicious on a mammogram?
hyperdense regions
microcalcifications
