Gynecology Flashcards

1
Q

precocious puberty- age cut-off

A

before age 8 in girls
before age 9 in boys

does not always have to be treated if not serious or impactful

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2
Q

precocious puberty causes

A

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

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3
Q

precocious puberty isosexual vs heterosexual

A

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

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4
Q

precocious puberty isosexual vs heterosexual

A

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

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5
Q

precocious puberty causes

A

familial/genetic (nonpathologic)

central (True) precosious puberty: early activation of hypothalamic pituitary- gonadal axis

pseudoprecocios puberty: autonomous excess secretion of sex steroids

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6
Q

precocious puberty isosexual vs heterosexual

A

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

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7
Q

pregesterone

A
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)

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8
Q

bHCG

A

maintains corpus luteum and progesterone secretion

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9
Q

mean age of menarch in the US

A

13

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10
Q

pregesterone

A

pro-gestation

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11
Q

True precocious puberty

A

high LH and FSH
GnRH will increase FSH further

treat by inducing menopause with continuous GnRH analog

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12
Q

mean age of menarch in the US

A

13

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13
Q

Pseudoprecocios puberty

A

low LH and FSH

no response when GnRH given

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14
Q

True precocious puberty

A

high LH and FSH

GnRH will increase FSH further

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15
Q

how long is luteal phase

A

13-14 days

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16
Q

FSH triggers release of which hormone from follicle?

A

estradiol

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17
Q

Menopause

A

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)

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18
Q

Premature ovarian failure:

A

amenorrhea for at least 1 year before age 40, or high FSH + menstrual irregularity before age 40

tobacco
radiation
chemo
abdominal disorders
pelvic surgery
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19
Q

Perimenopause

A

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

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20
Q

Menopause symptoms

A
hot flashes
breast pain
sweating
fatigue
anxiety/depression
dyspareunia
urinary frequency and dysuria
changes in bowel habits
vaginal atrophy
bladder symptoms
stress urinary incontinence
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21
Q

Menopause treatment

A

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

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22
Q

Pros and cons of hormone replacement therapy for menopause

A

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
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23
Q

Non-hormonal options for treating hot flashes

A
  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
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24
Q

Side effects of estrogen therapy

A
weight gain
nausea
breast tenderness
headache
endometrial proliferation
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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
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3 meds often used to treat ileus
erythromycin neostigmine metoclopramide
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Treatment for squamous cell cancer of the vagina
stage 1 (2cm): external beam radiation Stage 2, 3, 4: external beam radiation +/- adjuvant therapy (RADIATION)
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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
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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
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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
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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)
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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
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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
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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
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psammoma bodies
Serous cystadenocarcinoma
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estrogen excess
Granulosa-theca cell tumor
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androgen secretion
Sertoli-Leydig cell tumor
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diastolic murmur heard best in left lower sternum that increases with inspiration
tricuspid stenosis
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late diastolic murmur with an opening snap (no change with inspiration)
mitral stenosis
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systolic murmur heard best in the second right interspace
aortic stenosis
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systolic murmur heard best in the second left interspace
pulmonic stenosis
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Late systolic murmur best heard at the apex
mitral prolapse
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diastolic murmur with a widened pulse pressure
aortic regurgitation
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holosystolic murmur louder with inspiration at the left lower sternum
tricuspid regurgitation
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holosystolic murmur heard at the apex, radiates to the axilla
mitral regurgitation
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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 ```
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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)
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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
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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
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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
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Phyllodes tumor
large, bulky tumor more common in women in their 50s leaflike cleft:generally benign, can become malignant
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most common tumor in teen and young women
fibroadenoma
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most common mass in patients 25-50
fibrocystic change
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presents with serous or bloody nipple discharge
intraductal papilloma
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What gene mutation is commonly seen in men with breast cancer?
BRCA2 mutation
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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 ```
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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
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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
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Ductal carcinoma in situ (DCIS)
malignancy arising from duct without invasion precancerous Treatment: lumpectomy + possibly radiation mastectomy if high risk
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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
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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
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infiltrating lobular carcinoma
less fibrous than ductal (palpable, firm, fixed) often multifocal bilateral slower growing, slower to metastasize
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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
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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
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Hormone therapy in breast cancer
Always look for these three receptor types: estrogen and progesterone receptors HER2/Neu: trastuzumab (hereptin) ab against those receptors
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BRCA mutation PPX
b/l ppx mastectomies and oophorectomies to reduce risk of breast cancer and ovarian cancer later in life
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Breast cancer complications
``` mets: bone thorax brain liver ``` lymphedema: wound healing, infection, ROM, pain
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most common breast cancer
invasive ductal carcinoma
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what findings are suspicious on a mammogram?
hyperdense regions | microcalcifications