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Flashcards in Gynecology Deck (148):
1

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

2

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

3

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

4

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

5

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

6

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

7

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)

8

bHCG

maintains corpus luteum and progesterone secretion

9

mean age of menarch in the US

13

10

pregesterone

pro-gestation

11

True precocious puberty

high LH and FSH
GnRH will increase FSH further

treat by inducing menopause with continuous GnRH analog

12

mean age of menarch in the US

13

13

Pseudoprecocios puberty

low LH and FSH
no response when GnRH given

14

True precocious puberty

high LH and FSH
GnRH will increase FSH further

15

how long is luteal phase

13-14 days

16

FSH triggers release of which hormone from follicle?

estradiol

17

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)

18

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

19

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

20

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

21

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

22

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

23

Non-hormonal options for treating hot flashes

1. Venlafaxine- a good choice if any depression, anxiety, fatigue, isolation. Good first- line drug

2. Desvenlafaxine: only non-hormonal drug that is FDA-approved for hot flashes. Also works as an antidepressant

3. Clonidine- a good choice if BP control is also needed. SE- dry mouth, constipation, drowsiness

4. Gapabentin- good choice if insomnia, restless leg syndrome, seizure d/o, neuropathy, chronic pain

5. Time- about 30-50% of women have symptoms improvement within a few months, and most have resolution within 4-5 years

6. Placebo: placebo effect is about 20-25% effective in reducing hot flashes

24

Side effects of estrogen therapy

weight gain
nausea
breast tenderness
headache
endometrial proliferation

25

Side effects of progesterone therapy

acne
depression
hypertension

26

Primary Amenorrhea

16yo with normal secondary sex characteristics but no menses

13yo with absence of both menses and secondary sex characteristics

27

Causes of primary amenorrhea

hypothalamic or pituitary dysfunction

anatomic abnormalities
-absent uterus
-vaginal septum
-imperforate hymen

chromosomal abnormalities with gonadal dysgenesis
-Turner syndrome (45XO)

28

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

29

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

30

Labs to check in amenorrhea

1.
beta HCG
Thyroid studies (TSH and free T4)
Prolactin
FSH and LH
Androgens
-testosterone and DHEA

2.
progesterone challenge
estrogen-progesterone challenge

31

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

2. estrogen-progesterone challenge

32

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

33

What are the basics of a workup of primary amenorrhea

1. congenital defects: imperforate hymen, transverse vaginal septum, vaginal agenesis

2. if signs of hyperandrogenism, serum testosterone and DHEAS to assess for androgen- secting tumor

3. if galactorrhea, then serum prolactin and thyrotropin to assess for prolactinoma

If physical exam shows possible absence of uterus, then obtain a pelvic sonogram

4. 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)

5. 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

34

Labs to order for secondary amenorrhea

1. serum bHCG to rule out pregnancy
2. thorough H and P
3. serum prolactin (rule out hyperprolactinemia), serum TSH (rule out thyroid disease), serusm FSH (rule out ovarian failure)
4. If signs of hyperandrogenism, then serum DHEAS and total tetosterone
5. 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)

35

Treatment for amenorrhea

1. modify behavior
2. surgical correction
3. GnRH or gonadotropin replacement- Leuprolide
4. Dopamine agonists
5. hormone replacement therapy for symptom management
6. Lysis of adhesions and estrogen administration if Asherman syndrome

36

Primary dysmenorrhea

inflammation/trauma of shedding of endometrial lining

crampy lower abdominal pain
n/v
HA
diarrhea
mild tenderness

37

Secondary dysmenorrhea

Endometriosis
PID
Fibroids
Cysts
Adenomyosis

38

Risk factors for dysmenorrhea

menorrhagia
menarche

39

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

40

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)

41

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

42

Adenomyosis

growth of endometrial tissue within uterine wall

painful

43

The 3 Ds of endometriosis

dysmenorrhea
deep dyspareunia
dyschezia

44

Common causes of abnormal uterine bleeding

fibroids
cancer
HPO dysfunction
clotting disorders-von Willebrand disease
Threatened abortion
Molar pregnancy
Ectopic pregnancy

45

PALM-COEIN causes of abnormal uterine bleeding

PALM-COEIN
polyp
adenomyomas
leiomyoma
malignancy and hyperplasia
coagulopathy
ovulatory dysfunction
endometrial iatrogenic
not yet classified

46

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

47

How long is a menstrual cycle, typically?

21-35 days

48

polymenorrhea

49

oligomenorrhea

menstrual cycle >35 days

50

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

51

menorrhagia

Excessive bleeding

52

Metrorhagia

frequent bleeding

53

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

54

Bleeding related to intercourse

cervical lesion or polyp
glandular tissue on cervix

55

MCC AUB

ovulatory dysfunction

56

AUB and positive bHCG, + intrauterine pregnancy and closed os

threatened abortion

57

AUB and enlarged uterus + menoetrorrhagia for months

fibroids, molar pregnancy, adenomyosis

58

AUB and bleeding associated with severe menstrual pelvic pain

endometriosis, adenomyosis

59

AUB and menorrhagia in a perimenopausal woman

endometrial cancer or hyperplasia

60

AUB started with menarche

coagulopathy, vWF

61

AUB and positive bHCG+ severe pain + no fetus in uterus on US

ectopic pregnancy

62

AUB and metrorrhagia especially after intercourse + no pain + normal-sized uterus

polyp or glandular tissue on cervix

63

AUB and depression and constipation and abnormal uterine bleeding

hypothyroidism

64

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

65

indications for endometrial biopsy

over 45yo
multiple risk factors for endometrial cancer
persistent abnormal uterine bleeding > 6 months

66

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)

67

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

68

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)

69

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

70

lab findings consistent with PCOS

increased LH (LH:FSH ratio > 2:1)
increased testosterone
increased DHEA
increased androstenedione

71

When can lactation be an effective form of contraception

if

72

Vaginitis- what are the 3 main types?

bacterial vaginosis
trichomoniasis
fungal vaginitis

73

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

74

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

75

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

76

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)

77

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

78

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

79

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

80

Argyll-Robertson pupil

will constrict on accomodation but not on direct light

81

Genital herpes

HSV2
first outbreak is largest, with recurrences smaller, painful, usually in the same place

82

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

83

HPV cervical cancer

16 and 18: cervical cancer

penile, anal, head and neck cancer

Pap smear

84

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

85

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

86

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

87

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

88

Treatment: Gonorrhea

Ceftriaxone

89

Treatment: chlamydia

Doxycycline, azythromycin

90

Culture negative cystitis

suspect chlamydia

91

Anticholinesterases, organophosphates

atropine, pralidoxime

92

Abnormal uterine bleeding

beta HCG
Pap
wet prep
GC probe
CBC
bleeding time
PT/INR
PTT
TSH
Endometrial biopsy

93

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)

94

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

95

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)

96

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

97

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

98

Atypical squamous cells cannot exclude HSIL (ASC-H)

colposcopy

99

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

100

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)

101

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

102

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

103

Indications for EMBX

Age >35
-menometrorrhagia
-postmenopausal bleeding

Age

104

varicocele that does not empty when the patient is recumbent

renal cell carcinoma

105

3 meds often used to treat ileus

erythromycin
neostigmine
metoclopramide

106

Treatment for squamous cell cancer of the vagina

stage 1 (2cm): external beam radiation

Stage 2, 3, 4: external beam radiation +/- adjuvant therapy


(RADIATION)

107

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

108

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

109

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

110

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)

111

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

112

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

113

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

114

psammoma bodies

Serous cystadenocarcinoma

115

estrogen excess

Granulosa-theca cell tumor

116

androgen secretion

Sertoli-Leydig cell tumor

117

diastolic murmur heard best in left lower sternum that increases with inspiration

tricuspid stenosis

118

late diastolic murmur with an opening snap (no change with inspiration)

mitral stenosis

119

systolic murmur heard best in the second right interspace

aortic stenosis

120

systolic murmur heard best in the second left interspace

pulmonic stenosis

121

Late systolic murmur best heard at the apex

mitral prolapse

122

diastolic murmur with a widened pulse pressure

aortic regurgitation

123

holosystolic murmur louder with inspiration at the left lower sternum

tricuspid regurgitation

124

holosystolic murmur heard at the apex, radiates to the axilla

mitral regurgitation

125

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

126

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)

127

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

128

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


129

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

130

Phyllodes tumor

large, bulky tumor
more common in women in their 50s

leaflike cleft:generally benign, can become malignant

131

most common tumor in teen and young women

fibroadenoma

132

most common mass in patients 25-50

fibrocystic change

133

presents with serous or bloody nipple discharge

intraductal papilloma

134

What gene mutation is commonly seen in men with breast cancer?

BRCA2 mutation

135

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

136

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

137

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

138

Ductal carcinoma in situ (DCIS)

malignancy arising from duct without invasion

precancerous

Treatment:
lumpectomy + possibly radiation
mastectomy if high risk

139

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

140

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

141

infiltrating lobular carcinoma

less fibrous than ductal (palpable, firm, fixed)

often multifocal
bilateral
slower growing, slower to metastasize

142

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

143

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

144

Hormone therapy in breast cancer

Always look for these three receptor types:

estrogen and progesterone
receptors

HER2/Neu: trastuzumab (hereptin) ab against those receptors

145

BRCA mutation PPX

b/l ppx mastectomies and oophorectomies to reduce risk of breast cancer and ovarian cancer later in life

146

Breast cancer complications

mets:
bone
thorax
brain
liver

lymphedema: wound healing, infection, ROM, pain

147

most common breast cancer

invasive ductal carcinoma

148

what findings are suspicious on a mammogram?

hyperdense regions
microcalcifications