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Obstetrics and Gynecology > General gynecology > Flashcards

General gynecology Flashcards

1
Q

what is labial fusion

A

congenital anomaly

associated with excess androgens

develop abnormal genitalia

treat with estrogen cream

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2
Q

what is imperforate hymen and how do you treat it

A

congenital abnormality

junction between the sinovaginal bulb and the UG sinus is not perforated

obstructs flow

manifests as primary amenorrhea at puberty, hematocolpos (blood behind hymen)

tx is surgery

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3
Q

what are vaginal septums

A

congenital anomaly

when vagina forms, sinovaginal bulbs and mullerian tubercles must be canalized –> if not, you get a transverse vaginal septum between the lower 2/3 and upper 1/3

leads to primary amenorrhea

treat with surgery

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4
Q

how do you treat the congenital anomaly of vulvar hypertrophy

A

you get raised white lesions from irritation–> treat with cortisone cream BID

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5
Q

what is a bartholin’s cyst and how do you treat it

A

at 4 or 8 oclock on the labia minora

treat with sitz baths

if infected, do I and D or word catheter

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6
Q

what causes fibroids

A

estrogen dependent local proliferation of smooth muscle cells, usually in women of child bearing age and then they regress at menopause

has pseudocapsule of compressed muscle cells

are found in 20-30% of american women at age 30

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7
Q

what population is at higher risk for uterine fiberoids

A

african american women

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8
Q

signs and symptoms of fibroids

A

menorrhagia (submucous)

metrorrhagia (subserous, intramural)

pressure symptoms (from pressing against bladder)

infertility

50% are asymptomatic

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9
Q

what are parasitic fibroids

A

get their blood supply from the omentum

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10
Q

what histologic changes can be associated with fibroids

A

hyaline change

cystic change

calcific change

fatty change

red/white infarcts

sarcomatous change (most rare)

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11
Q

what are the risks associated with fibroids in pregnancy

A

spontaneous abortion

IUGR

PTL

dystocia

fibroids may grow during pregnancy

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12
Q

what are the medical treatment options for fibroids

A

depo provera

lupron (GnRH antagonist)

danazol

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13
Q

what are the surgical treatment options for fibroids

A

momectomy (only for fertility purposes)

hysterectomy is indicated if anemic from bleeding, severe pain, size above 12, urinary frequency, growth after menopause

there is a new role for embolization with IR

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14
Q

define endometrial hyperplasia

A

abnormal proliferation of gland/stromal elements and overabundance of HISTOLOGICALLY NORMAL epithelium

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15
Q

what is the risk of cancer, and how do you treat, endometrial hyperplasia that is:
simple without atypia

A

1% cancer

provera

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16
Q

what is the risk of cancer, and how do you treat, endometrial hyperplasia that is:
complex without atypia

A

3% cancer

provera

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17
Q

what is the risk of cancer, and how do you treat, endometrial hyperplasia that is:
simple with atypia

A

9% cancer

provera versus hysterectomy

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18
Q

what is the risk of cancer, and how do you treat, endometrial hyperplasia that is:
complex with atypia

A

27% cancer

hysterectomy

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19
Q

what are risk factors that predispose you to endometrial hyperplasia

A

unopposed estrogen

PCO

granulosa/thecal tumours

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20
Q

how do you diagnose endometrial hyperplasia

A

endometrial biopsy

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21
Q

define adenomyosis

A

endometrium in myometrium

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22
Q

how does adenomyosis usually present

A

30 yo multiparous woman with HEAVY, PAINFUL periods

enlarged uterus that is either boggy/soft or woody/firm with pelvic heaviness

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23
Q

how do you treat adenomyosis

A

hysterectomy with analgesia

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24
Q

define pelvic endometriosis

A

presence of endometrial glands outside of endometrium

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25
Q

what are the theories of why pelvic endometriosis develops

A
  1. sampson’s reflux menstruation–> most likely
  2. coelomic metaplasia–> irritant to peritoneum
  3. family history/genetic
  4. immunologic
  5. lymphatics and vascular mets
  6. iatrogenic dissemination (ie see it on the other side of a C/S scar)
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26
Q

why do you do get pain with pelvic endometriosis

A

induces fibrosis which causes pain

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27
Q

signs and symptoms of pelvic endometriosis

A

pain

infertility

bleeding/ovarian dysfunction

hematochezia/hematuria

dyspareunia

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28
Q

where might you find endometrial tissue in a woman with pelvic endometriosis

A

peritoneum

ovary (“chocolate cysts”)

round ligament

fallopian tubes

sigmoid colon

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29
Q

how do you diagnose endometriosis

A

laparoscopy

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30
Q

how do you treat pelvic endometriosis

A

NSAIDS

OCP/provers

luprin (GnRH agonist)–> induces pseudomenopause

laser surgery/coagulation of implants

TAH/BSO

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31
Q

what is the usual cause of ovarian cysts

A

usually follicular from failure of follicle rupture–> often disappear within 60 days

3-8 cm

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32
Q

what are the types of ovarian cysts

A
  1. corpus luteum cysts–> firm/solid
  2. cystic/hemorrhagic–> hemoperitoneum
  3. theca lutein–> bilateral, filled with straw fluid, high beta hCG
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33
Q

how do you diagnose ovarian cysts

A

ultrasound

Ca125 in cases where ovarian cancer is suspected

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34
Q

what is the differential diagnosis for ovarian cysts

A

ectopic pregnancy

tuboovarian abscess

torsion

endometriosis

neoplasm

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35
Q

treatment for ovarian cysts

A

if premenopausal–> can observe if size is below 8 cm

if post menopausal (any size) or premenopausal above 8 cm–> needs laparoscopy vs. laparotomy for cystectomy or oophrectomy

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36
Q

how do you diagnose chlamydia trachomatis

A

direct fluorescence antibodies

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37
Q

how do you treat chlamydia trachomatis

A

doxycycline 100 mg BID for 7 days

-or-

azythromycin 1g PO (one dose)

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38
Q

how do you diagnose gonorrhea

A

gram stain and culture

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39
Q

what are the risk factors for gonorrhea

A

low socioeconomic status

urban

nonwhite

early sex

previous gonorrhea infection

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40
Q

how do you treat gonorrhea

A

treat both partners

Cipro 500 mg PO

usually transfers male to female more than female to male

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41
Q

what organism causes syphilis

A

treponema pallidum

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42
Q

how do you diagnose syphilis

A

dark field microscopy

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43
Q

how do you treat syphilis

A

if less than 1 year duration–> pen G 2.4 million U IM

if more than 1 year duration–> pen G 2.4 million U IM x 3 doses

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44
Q

how do you treat HSV

A

first episode–> acyclovir or valcyclovir

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45
Q

what is the natural history of HSV

A

of the genital eruptions, 66% are due to HSV 2 and 33% due to HSV 1

vesicles rupture in 10-22 days leaving a painful ulcer

can use antivirals also as suppressing agents as the virus hangs out in the dorsal root ganglion

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46
Q

what types of HPV cause genital warts

A

6 and 11

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47
Q

what types of HPV cause cervical cancer

A

16, 18, 31

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48
Q

what is the treatment for HSV

A

podofilox

cryotherapy

podophyllin rein

TCA

aldara cream

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49
Q

what is a chancroid

A

caused by haemophilus ducreyi

painful soft ulcer with inguinal LAD

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50
Q

how do you treat a chancroid caused by haemophilus ducreyi

A

ceftriaxone 250 IM once

-or-

azythromycin 1 g once PO

-or-

erythromycin

*treat partner

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51
Q

how does lymphogranuloma venerum present

A

primary–> papules/shallow ulcer

secondary–> painful inflammation of inguinal nodes with fever, headache, malaise, anorexia

tertiary–> rectal stricture, rectovaginal fistula, elephantitis

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52
Q

how do you treat lymphogranuloma venerum

A

doxycycline 100 mg PO BID for 21 days

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53
Q

what is molluscum contagiosum

A

pox virus from close contact

1-5 mm umbilicated lesions anywhere except for the palms or soles of feet

are asymptomatic and resolve on their own

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54
Q

what are risk factors for candida

A

antibiotic use

pregnancy

diabetes

immunocompromised

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55
Q

signs and symptoms of candida

A

burning, itching

vulvitis

cottage cheese discharge

dyspareunia

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56
Q

how do you diagnose candida

A

wet prep with KOH shows BRANCHING HYPHAE

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57
Q

what do you see on exam for candida

A

white plaques with or without satellite lesions

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58
Q

how do you treat candida

A

over the counter creams work well (monistat)

if resistant–> DIFLUCAN 150 mg PO once

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59
Q

what organism causes trichomonas

A

unicellular flagellated protozoan

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60
Q

signs and symptoms of trichomonas

A

itching

increased discharge that is yellow/gray/green and frothy

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61
Q

what do you see on exam for trichomonas

A

strawberry cervix

foamy discharge

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62
Q

how do you diagnose trichomonas

A

“see the buggers zipping all over your wet prep”

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63
Q

how do you treat trichomonas

A

metronidazole 500 mg PO BID for 7 days

use a condom with partner for 2 weeks

*avoid metronidazole in first trimester

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64
Q

what organism causes bacterial vaginosis

A

gardnerella vaginalis

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65
Q

signs and symptoms of bacterial vaginosis

A

odorous discharge

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66
Q

how do you diagnose bacterial vaginosis

A

whiff test by adding KOH

see clue cells on wet prep (spotty squamous cells)

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67
Q

how do you treat bacterial vaginosis

A

metronidazole 500 mg BID for 7 days

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68
Q

is bacterial vaginosis and STI

A

no

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69
Q

what are the symptoms of vaginal atrophy

A

burning on sex

occurs post menopausal

treat with estrogen

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70
Q

what organisms cause PID

A 
neisseria
chlamydia
mycoplasma
ureaplasma
bacteroides
among others...
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71
Q

symptoms of PID

A 
diffuse lower abdo pain
vaginal discharge
bleeding
dysurina
dyspareunia
CMT
adnexal tenderness
GI discomfort
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72
Q

how do you diagnose PID

A

cervical motion tenderness

adnexal tendereness

discharge

fever

elevated WBC

elevated ESR

*mostly based on clinical exam

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73
Q

what labs should be ordered if PID suspected

A

cultures

pelvic U/S if mass is palpated

monitor WBCs

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74
Q

how do you treat PID

A

ceftriaxone 2 g IV q12, doxycycline 100 mg IV or clinda-genta

usually treat for 48 hours IV then if afebrile step down to doxycycline 100 mg PO BID for 14 days

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75
Q

what can be a complication of PID

A

tubo ovarian abscess (TOA)

persistent PID progresses to TOA in 3-16% of cases

presents as adnexal fullness/mass (not walled off like a true abscess)

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76
Q

how do you diagnose TOA

A

U/S

pelvic CT if obese

increased WBC with left shift and increased ESR

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77
Q

how do you treat TOA

A

hospitalize for IV abx–> triple therapy with ampicillin, gentamycin, clinda

if TOA ruptures or doesnt resolve–> surgery

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78
Q

what is toxic shock syndrome

A

vaginal infection not associated with menstruation

can be assoc with delivery, C/S, post partum endometritis, spontaneous abortion or laser treatment

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79
Q

what is the causative agent and process behind TSS

A

STAPH AUREUS produces epidermal TSS T-1 that produces fever, erythematous rash, desquamation of palmar surfaces and hypotension

can also see GI disturbance, malaise, mucous membrane hyperemia, change in mental status

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80
Q

what might you see on labs in TSS

A

increased BUN/Cr

decreased platelets

NEGATIVE BLOOD CX

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81
Q

treatment for TSS

A

ALWAYS HOSPITALIZE

may need ICU and IV fluids and/or pressors

antibiotics do not shorten the length of the acute illness but they do decrease the risk of recurrence

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82
Q

what type of muscle is the detrusor muscle and the urethra

A

smooth muscle

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83
Q

what is the innervation of micturition

A

PSNS–> S2, 3, 4 allows micturition via cholinergic receptors

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84
Q

what is the innervation of “holding” urine

A

SNS–> hypogastric nerves, T10-L2 prevents urination by contracting the bladder neck and internal sphincter via norepinephrine receptors

somatic control of external sphincter via pudendal nerve

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85
Q

what is the exam for pelvic relaxation defects caused

A

POP Q

stage 1–> prolapse upper 2/3 of vagina

stage 2–> to the level of the introitus

stage 3–> outside of the vagina

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86
Q

treatment for pelvic relaxation defects

A

kegels (contraction of levator ani)

estrogen replacement

vaginal pessaries

surgery

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87
Q

what causes urge incontinence

A

detrussor instability

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88
Q

symptoms of urge incontience

A

urgency

often cannot make it to bathroom

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89
Q

causes of urge incontinence

A

foreign body

UTI

stones

cancer

diverticulitis

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90
Q

diagnosis of urge incontinence

A

based on history

can be shown on urodynamic studies (catheter in bladder, rectum and machine to measure the difference…bladder is filled with NS and response to that filling is measured)

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91
Q

treatment for urge incontinence

A

kegel exercises

anticholingerics (ditropan, amytriptaline)

muscle relaxants

beta agonists

estrogen replacement

*surgery not used here, medical therapy more appropriate

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92
Q

what do urodynamic tests show in the setting of urge incontinence

A

involuntary/uninhibited bladder contraction

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93
Q

what are the symptoms of stress incontinence

A

involuntary loss of urine when there is increased abdo pressure mostly from sneezing, coughing, laughing which transmits pressure to the urethra

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94
Q

what is the mechanism of stress incontinence

A

intrinsic sphincter defect

hypermobile bladder neck

pelvic relaxation

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95
Q

what are the causes of stress incontinence

A

trauma

neuro dysfunction

associated with multiparity

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96
Q

treatment for stress incontinence

A

kegels

alpha agonists

estrogen cream

retropubic urethroplexy

trans vaginal tape procedure

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97
Q

what is a retropubic urethroplexy

A

surgery in which the periurethral tissue is joined with cooper’s ligament –> BURCH

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98
Q

what is a trans vaginal tape procedure

A

periurethral tissues are raise towards the abdo wall using a mesh sling placed under local anesthesia

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99
Q

symptoms of overflow incontinence

A

dribbling

urgency

stress

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100
Q

mechanism of overflow incontinence

A

underactive detrussor muscle leading to poor or absent bladder contractions

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101
Q

causes of overflow incontinence

A

DM

drugs

fecal impaction

MS

neuro impairment

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102
Q

treatment for overflow incontinence

A

treat underlying cause

Hytrin

bethanechol

intermittent catheterization

dantroleen

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103
Q

diagnosis of overflow incontinence

A

urodynamic studies

post void residual scan (over 100 cc is abnormal)

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104
Q

what are the risk factors for urinary fistula

A

PID

radiation

endometriosis

prior surgery

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105
Q

what are the symptoms of urinary fistula

A

produces continuous urine leakage commonly following pelvic surgery/radiation

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106
Q

how do you diagnose urinary fistula

A

methylene blue dye injection into the bladder –> place tampon in vagina–> if there is a vesicovaginal fistula, tampon will be blue

indigo carmine due given IV with tampon in vagina–> if ureterovaginal fistula, tampon will be blue

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107
Q

treatment for urinary fistula

A

surgery–> must wait 3-6 months to repair post surgical fistulas

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108
Q

what happens during puberty

A

secondary sex characteristics develop

growth spurt

achievement of fertility

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109
Q

define adrenarche

A

6-8 years old

regenerates zona reticularies that produces DHEA-S, DHEA and androsteinone

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110
Q

define gonadarche

A

pulsatile GnRH secretion goes into anterior pituitary to secrete LH, FSH

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111
Q

define thelarche

A

around age 11

breast formation–> tanner stages

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112
Q

define pubarche

A

around 12 years old

pubic hair and axillary hair development

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113
Q

when do girls usually have their growth spurt

A

age 9-13

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114
Q

what happens during the growth spurt

A

increase GH and somatomedian-C result in peak height velocity, increased estrogen levels, fusion of growth plates

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115
Q

when does menarche usually occur

A

ages 12-13

anovulatory period of up to 1 year

may take 2 years to have regular cycle

delayed in athletes

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116
Q

what is a pneumonic to remember the tanner stages in women

A

boobs pubes pits pads (breast, hair, grow, bleed)

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117
Q

what are the tanner stages of the breast

A
  1. prepubertal
  2. breast bud
  3. breast elevation
  4. areolar mound
  5. adult contour
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118
Q

what are the tanner stages of hair

A
  1. prepubertal
  2. presexual hair
  3. sexual hair
  4. mid-escutcheon
  5. female escutcheon
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119
Q

what is menopause

A

cessation of menstruation

120
Q

when does menopause usually occur

A

ages 50-51

if below 40 years–premature
if below 35 years–premature ovarian failure

121
Q

what are the symptoms of menopause

A

irregular menses

hot flashes secondary to decreased estrogen

mood changes

depression

lower urinary tract atrophy

genital changes

osteoporosis

122
Q

what lab values indicate menopause

A

FSH above 40

elevated LH

decreased estrogen resulting in decreased negative feedback

123
Q

how do you diagnose menopause

A

history and physical

PE shows decreased breast size with vaginal, urethral and cervical atrophy due to decreased estrogen

124
Q

how do you treat the symptoms of menopause

A

HRT –> primarily estrogen and progesterone if patient has uterus

calcium

vit D

exercise to counter decreased osteoclast activity

estrogen cream to counter vaginal atrophy

125
Q

what are contraindications to HRT

A

vaginal bleeding

thromboembolic disease

breast ca

uterine ca

126
Q

why do we not recommend unopposed estrogen in women with a uterus

A

without progesterone, it can result in endometrial hyperplasia and cancer

127
Q

what are the consequences of decreased estrogen

A

unfavorable lipid profile that can result in stroke or MI

increased bone resorption because estrogen decreases osteoclast activity predisposing to fractures etc

atrophy and skin and muscle tone

128
Q

are there problems taking estrogen alone when u dont have a uterus

A

no

129
Q

what happens if an otherwise phenotypically normal female has a Y chromosome

A

Y chromosome makes mullerian inhibitory factor–> no uterus if MIF present

130
Q

what hormone is responsible for breast development

A

estrogen

131
Q

what is the problem in a women who has a uterus, but no breast development

A

NO ESTROGEN

if FSH high–> ovarian failure (hypergonadotropic hypogonadism)

  • -Turner’s is another cause–ovaries undergo rapid atresia
  • -can be mosaic
  • -can be due to 17 hydroxylase deficiency–> MIF is produced so no female internal organs
  • -can be due to pure gonadal dysgenesis

if FSH low–> insufficient GnRH, hypopituitarism, gonadal agenesis, 46 xy with testes not developing because MIF NOT released (external female genitalia but no breasts)

132
Q

what does 17 hydroxyalase deficiency cause

A

MIF is produced so no female internal organs

133
Q

what is the problem if a woman has breasts but no uterus

A

estrogen in the presence of MIF

Rokitansky Kuster Hauser–> uterovaginal agenesis with other anomalies (46xx)

Androgen insensitivity–> 46 xy; testicular feminization because no receptors for testosterone–> MIF is secreted therefore no mullerian structures

134
Q

what is the problem if there is no breasts or uterus

A

xy genotype–> i.e 17 hydroxylase deficiency

135
Q

what are some causes of primary amenorrhea

A

genetic–> turners, ovarian failure, 17 hydroxylase deficiency, hypopituitarism, rokitansky kuster hauser, androgen insensitivity

anatomic–> imperforate hymen, transvaginal septum, vaginal agenesis, no patent vagina

136
Q

what should you ask about in history for secondary amenorrhea

A

stresses

weight loss or gain

drugs

exercise

UPT

estradiol level

progesterone challenge

137
Q

what does bleeding with the progesterone challenge indicate? what should you check next?

A

that there is enough estrogen

check FSH, LH and PRL next

138
Q

if a patient with amenorrhea bleeds with the progesterone challenge and LH is high, what should you think?

A

PCO

139
Q

if a patient with amenorrhea bleeds with the progesterone challenge and LH is normal what should you think

A

hypothalamic amenorrhea–> stress, exercise, post pill

140
Q

if a patient with amenorrhea bleeds with the progesterone challenge and prolactin is increased, what should you think

A

prolactinoma

hypothyroid

pregnancy

141
Q

what does no bleeding on progesterone challenge indicate

A

no estrogen

check FSH, LH, PRL

142
Q

if a patient with amenorrhea does not bleed with progesterone challenge, and FSH is high, what should you think

A

ovarian failure or resistant ovarian syndrome

143
Q

if a patient with amenorrhea does not bleed with progesterone challenge, and FSH is low or normal what should you think

A

check MRI/CT for pituitary tumous, sheehan’s syndrome

144
Q

other than hormonal causes, what can cause secondary amenorrhea

A

ashermans after D and C

cervical stenosis after CKC

145
Q

what is Swyer’s syndrome

A

46 xy

gonado-agenesis

no testes

no MIF

yields female genitalia but no breasts because no estrogen

146
Q

what is Kallmans syndrome

A

absence of GnRH and anosomia

patients have breasts and uterus

147
Q

what is testicular feminization

A

46xy

insensitive to testosterone

MIF so no internal female genital structures

has estrogen so has breasts

148
Q

what are the probable causes of PMS

A

abnormal estrogen/progesterone balance

increased PG production

decreased endogenous endorphins

disturbance in RAAS sysytem

149
Q

how do you diagnose PMS

A

5 of 12 symptoms, including one of first 4:

  1. decreased mood
  2. anxiety
  3. affective lability
  4. decreased interest
  5. irritability
  6. concentration difficulty
  7. decreased energy
  8. change in appetite
  9. overwhelmed
  10. edema
  11. weight gain
  12. breast tenderness
150
Q

when does PMS occur

A

second 1/2 of cycle

151
Q

what are some ways to mitigate the effects of PMS

A

avoid caffeine, alcohol, tobacco

low sodium diet

weight reduction

stress management

drugs–> NSAIDS, OCPs, lasix, calcium, vitamin E, SSRI

152
Q

what is dysmenorrhea

A

pain and cramping during menstruation that interferes with acts of daily living

153
Q

what is primary dysmenorrhea

A

presents at age below 20 years because of increased PG occurring with ovulatory cycles

154
Q

what is secondary dysmenorrhea

A 
endometriosis
adenomyosis
fibroids
cervical stenosis
adhesions
155
Q

what is menorrhagia

A

heavy prolonged menstrual bleeding

over 80 mL per cycle (average is 35 mL)

more than 24 pads per day

156
Q

what can cause abnormal uterine bleeding

A 
fibroids
adenomyosis
endometrial hyperplasia
endometrial polyps 
cancer
pregnancy complications
157
Q

how should you manage AUB in a pubertal girl

A

give Fergon, NSAIDS and premarin until bleeding stops

check vWF

158
Q

how do you manage AUB in a 16-40 year old woman

A

think endometriosis, adenomyosis, fibroids

EMB, OCPs

159
Q

how do you manage AUB in over 40 year old woman

A

endometrial cancer

treat with EMB, depo provera, D and C, TAH

160
Q

define metrorrhagia

A

intermenstrual bleeding

think endometrial polyps, endometrial/cervical cancer, pregnancy complication

161
Q

define polymenorrhea

A

cycles are less than 21 days between periods

anovulation

162
Q

define oligomenorrhea

A

cycles more than 35 days apart

due to disruption of gonadal pituitary axis or pregnancy

163
Q

what are the causes of ovulatory bleeding

A

early–> estrogen is not increasing fast enough

mid–> estrogen drop off at ovulation

later–> progesterone deficiency

treat with NSAIDs which can decrease blood loss by 20-50%

164
Q

how do you diagnose hirsutism/virilism

A

assess body hair systematically–> hair type is villus hairs which cover the entire body or terminal hairs become thick

free testosterone–> the OVARY produces the most testosterone

DHEAS–> ADRENAL produces the most DHEAS, screens for adrenal tumours

17 hydroxy progesterone–> CAH

165
Q

define symptoms of hirsutism

A

increase in terminal hairs especially on face, chest, back

diamond shaped escutcheon in male

increased 5 alpha reductate

166
Q

define symptoms of virilism

A

male features

deepening of voice

balding

increasing muscle mass

clitoromegaly

breast atrophy

male body habitus

167
Q

possible causes of virilism/hirsutism

A

adrenal tumours

ovarian tumour

PCOS

cushings–> increases ACTH, cortisol

CAH–> 21 and 11 hydroxylase deficiency

168
Q

what is PCOS

A

can include numerous ovarian cysts but is more than that–> includes:

insulin resistance (diagnosed by fasting glucose/insulin ratio less than 4.5)

hirsutism (from hyperandrogenemia)

anovulation (irregular heavy periods)

FSH: LH ratio above 2.5:1

169
Q

how do you treat PCOS

A

metformin for insulin resistance

clomid for anovulation (if desires fertility)

170
Q

define infertility

A

inability to achieve pregnancy after 12 months of unprotected intercourse

171
Q

what are the causes of infertility

A

idiopathic–> 10%

male and female–> 10%

female causes–> 40%

male causes–> 40%

172
Q

what are the categories of female causes of infertility

A
  1. ovulatory
  2. tubal
  3. peritoneal
  4. uterine
  5. luteal phase defect
173
Q

what are some of the ovulatory causes of infertility

A

anovulation

endocrine

PCOS

premature ovarian failure

174
Q

how do you manage ovulatory causes of infertility

A

ovulation induction–> 70% success

CLOMID–> antiestrogen that results in increased FSH, more mature follicles and ovulation (side effects hot flashes, emotional lability, depression, multiple gestation)

PERGONAL–> purified FSH/LH HMG IM injection in follicular phase (85-90% effective)

IVF, GIFT, ZIFT–> ovulation induction, harvest oocytes, add sperm, fertilize, place in uterus

175
Q

what are some tubal causes of infertility

A

adhesions

endometriosis

PID

salpingitis

176
Q

how do you manage tubal causes of infertility

A

tubal reconstruction

177
Q

what are some peritoneal causes of infertility

A

endometriosis

adhesions

PID

178
Q

what are some uterine causes of infertility

A

asherman’s

fibroids

179
Q

how do you treat uterine causes of infertility

A

myomectomy for fibroids

180
Q

how do you treat luteal phase defects

A

progesterone during and after conception

181
Q

what are some male causes of infertility

A

cryptocordism

varicocele

epidydimitis

prostatitis

182
Q

how do you manage male causes of infertility

A

intrauterine insemination

183
Q

what are some meds that can decrease male fertility

A

cimetidine

colchicines

sulfalazine

allopurinol

erythromycin

steroids

tetracycline

184
Q

what is the work up for infertility

A

sperm count–> FIRST

TSH, prolactin

HSG–> assess tubal patency and diagnose intrauterine defects

post coital test–> quality of mucus and sperm, done on day 12-14

BBT-temperature curve–> spike predictive of ovulation

progesterone day 21 level to assess ovulation

diagnostic scope to look for endometriosis

185
Q

what is lichen sclerosis

A

thin skin, hyalinized collaged in the vulva

white plaques

186
Q

how do you treat vaginal lichen sclerosis

A

clobetasol (high potency steroid)

187
Q

what is extramammary paget’s disease

A

intraepithelial neoplasia of the vulvar skin

find it in women over 60 with vulvar purities

presents as pale atypical cells with mitotic figures

20% have adenoca underneath

188
Q

what are the symptoms of extramammary paget’s disease

A

pruritus unrelieved by anti-fungals

189
Q

how do you diagnose extramammary paget’s disease

A

biopsy

190
Q

how do you treat extramammary paget’s disease

A

wide local excision, colposcopy

191
Q

why do we care about extramammary paget’s disease

A

20% have adenocarcinoma underneath

associated with other cancers–> GI, breast, cervical and with chronic inflammatory changes

scare yields red velvet and white plaques on labia

infranodal spread likely to be fatal

192
Q

what is vulvar intraepithelial neoplasia

A

“VIN–> I, II or III”

dysplasia of the vulva

atypical, thickened skin

degree is proportioned to the number of mitotic figures

can see squamous pearls

193
Q

in what population is VIN most common

A

post menopausal ages 50-60

194
Q

what virus is correlated with VIN most of the time

A

HPV 80-90% of the time

195
Q

what are the symptoms of VIN

A

diffused focal raised or flat white, red, brown or black lesions

vulvodynia

pruritus

196
Q

treatment of VIN

A

excision with scalpel or laser

f/u colposcopy every 3 months until disease free then every 6 mo

197
Q

what % of gyne malignancies are vulvar

A

5%

198
Q

what other diseases are associated with vulvar cancer

A

DM

HTN

obesity

vulvar dystrophies

199
Q

symptoms of vulvar ca

A

vulvodynia

pruritus

mass –> cauliflower look, hard, indurated

erythema

200
Q

how do you diagnose vulvar ca

A

biopsy–> see EPIDERMOID in 90% of cases

melanoma 5-10%

basal 2-3%

201
Q

how do you stage vulvar ca

A

I–> less than 2 cm, no nodes, no mets (Ia is less than 1mm)

II–> over 2 cm, no nodes, no mets but can progress to perineum, urethra and anus

III–> unilateral nodes of any size

IV–> bilateral nodes, mets

202
Q

how do you treat vulvar ca

A

based on stage

ranges from wide local excision to vulvectomy to radical vulvectomy/lymph node dissection

203
Q

what population is at highest risk of vaginal ca

A

women in their 50s

204
Q

what % of paps may be false negative

A

40-50%

lower in BC because centralized

205
Q

what do “benign cellular changes” mean on an abnormal pap

A

think infection–wet prep and cultures are next step

206
Q

what does “koilocytosis” mean on an abnormal pap

A

pathologic description associated with HPV

207
Q

what does “ASCUS” mean on an abnormal pap

A

atypical squamous cell hyperplasia of undetermine significance

5% hide underlying severe lesions

repeat pap in 3 months, colposcopy is 2 come back as ASCUS

consider HPV typing

208
Q

what does “LGSIL” mean on an abnormal pap

A

low grade squamous intraepithelial lesion

treat with colposcopy

209
Q

what does “HGSIL” mean on an abnormal pap

A

high grade squamous intraepithelial lesion

treat with colposcopy

210
Q

what is a colposcopy

A

magnifies region of the cervix after stained with acetic acid

areas of dysplasia stain WHITE (aceto white focal lesion) and are biopsied

an endocervical curretage is also done

211
Q

how do you treat cervical dysplasia

A

based on biopsy and ECC result

212
Q

how do you treat mild cervical dysplasia

A

observation and cryotherapy

213
Q

how do you treat moderate cervical dysplasia

A

cryotherapy or LEEP

214
Q

how do you treat severe cervical dysplasia

A

LEEP or cold knife conization (CKC)

215
Q

list the 4 indications for CKC

A

microinvasion on biopsy

ECC with dysplasia

pap colpo discrepancy–> if pap smear does not correlate with the biopsy results i.e HGSIL with normal biopsy, you may have missed something and need to do CKC

inadequate colpo–> means there is a lesion extending into the os or that you could not visualize the whole lesion on colpo and may be something more extensive

216
Q

what is ECC

A

endocervical curretage

217
Q

where does most cervical cancer occur

A

transformation zone

218
Q

what is a koilocyte

A

has a viral particle

assoc with HPV

219
Q

which HPV types are oncogenic

A 
33
35
52
16
18
220
Q

which HPV types cause warts

A

6

11

221
Q

what are the symptoms of cervical cancer

A

vaginal bleeding

discharge

pelvic pain

growth on cervix

may palpate or see mass on exam

222
Q

what is the classic presentation of cervical ca

A

post coital bleeding

pelvic pain/pressure

abnormal vaginal bleeding

rectal or bladder sx

223
Q

what are the types of cervical cancer

A

squamous large cell

keratinizing

non keratinizing

small cell (worst prog)

adenocarcinoma

mixed carcinoma

glassy cell–> pregnancy women, usually fatal

224
Q

risk factors for cervical ca

A

tobacco

multiple sexual partners

age of onset of sex

number of STDs

HIV (cervical ca is an AIDS defining disease)

225
Q

how do you stage cervical ca

A

based on microinvasion so MUST DO A CONE BIOPSY

0–> carcinoma in situ

I–> contained to cervix

II–> carcinoma beyond cervic, no sidewall

III–> pelvic sidewall, hydronephrosis

IV–> extends beyond pelvis

226
Q

treatment of stage Ia cervical ca

A

cone biopsy, hysterectomy 100% cure

227
Q

treatment of stage Ib/IIa cervical ca

A

radiation, radical hysterectomy (cervix, uterus, parametrium, LN)

228
Q

treatment for stages IIb/III/IV cervical ca

A

extensive radiation and chemo

229
Q

risk factors for ovarian tumours

A

family history

uniterrupted ovulation

nulliparous

low fertility

delayed childbearing

late onset menopause (OCPs have protective effects)

230
Q

symptoms of ovarian tumours

A

asymptomatic until advanced stages

urinary frequency, dysuria, pelvis pressure, ascites

231
Q

what are the types of ovarian tumours

A
  1. non neoplastic
  2. epithelial (80%)
  3. germ cell
  4. stromal
  5. other
232
Q

how do you treat non neoplastic ovarian tumours

A

only operate if post menopausal or if greater than 8 cm

233
Q

what are the types of non neoplastic ovarian tumours

A

follicle cyst

corpus luteum hematoma

PCOS

theca lutein cysts

endometrioma

para ovarian cysts (mullerian)

234
Q

what is the most common type of ovarian tumour

A

epithelial

235
Q

what are the types of epithelial ovarian tumours

A
  1. serous cystadenoma–> papillary, cystic, malignant, bilateral–> PSAMMOMMA BODIES
  2. endometroid–> solid
  3. mucinous–> cystic
  4. clear cell–> associated with HOBNAIL CELLS on path, association with DES
  5. Brunner–> look like transitional epithelium
  6. SUET–> solid, undifferentiated
236
Q

what are the types of germ cell ovarian tumours

A
  1. dysgerminoma–> younger people, solid, radiosensitive, lymphocytic infiltrate
  2. teratoma–> ectoderm, endoderm, mesoderm; rotikansky’s protuberance
  3. primary chriocarcinoma of the ovary
  4. yolk sac tumour/endodermal sinus
  5. mixed germ cell
237
Q

what are the medical complications of ovarian teratomas

A

struma ovarii

autoimmune hemolytic anemia

carcinoid syndrome

238
Q

what are the surgical complications of ovarian teratomas

A

torsion

acute abdo

239
Q

what tests will be positive in primary choriocarcinoma of the ovary

A

false positive UPT

increased beta hCG

240
Q

what tests will be positive in yolk sac/endodermal sinus ovarian tumours

A

AFP/LDH

schuller duval bodies

241
Q

what tests will be positive in mixed germ cell ovarian tumours

A

HCG

AFP

LDH

Ca 125

242
Q

what population is associated with stromal ovarian tumours

A

50-80 years old

243
Q

what is the defining feature of a stromal ovarian tumours

A

hormone production

244
Q

what are the types of stromal ovarian tumours and what are their symptoms

A
  1. fibroma–> Meig’s syndrome (ovarian tumour, right hydrothorax, ascites)
  2. granulosa theca–> feminizing, late recurrence, Call Exner bodies, produce large amounts of estrogen
  3. sertoli leidig–> masculinizing, secrete testosterone, crystaloids of reinke secrete androgens
  4. gynadroblastoma–> components of male and female
245
Q

how do you stage ovarian cancer

A

I–> growth to one or both ovaries

II–> extension to pelvic structures

III–> peritoneum

IV–> distant mets

246
Q

what chemo is used in ovarian ca

A

cisplatin and taxol

247
Q

what blood test is elevated in most ovarian cancers

A

Ca125–> follow

248
Q

what are the characteristics of cancer of the fallopian tubes

A

adenoca from mucosa

disease progresses like ovarian ca

peritoneal spread

ascites

bilateral in 10-20% results from mets often

primary is very rare

asymptomatic but may have vague lower abdo pain and discharge

249
Q

treatment for fallopian tube ca

A

TAH/BSO

cisplatin

cyclophosphamide XRT

250
Q

define complete trophoblastic molar pregnancy

A

less than 20 years or above 40 years

80% of molar pregnancies are complete

worse because can transform into malignant (20%)

no baby parts

251
Q

define incomplete trophoblastic molar pregnancy

A

triploid (usually XXY)

may have baby parts

252
Q

symptoms of trophoblastic molar pregnancy

A

early abnormal bleeding

large for dates

bilateral enlarged ovaries

increased in asians

early toxemia

threatened abortion

hyperemesis, hyperthyroid, HTN

253
Q

risk factors for molar pregnancy

A

maternal age

history of hyaditiform mole

recurrent SAB

low SES

poor nutrition

254
Q

treatment of molar pregnancy

A

D and C

consider hysterectomy

255
Q

follow up for molar pregnnacy

A

monitor HCG for one year

contraception for one year (dont want to confuse rising HCG titers of new pregnancy with those from molar pregnancy)

pelvic exams every 2 weeks until uterus clear

chemo is HCG is icnreased at 6 mo, has lung or other mets or recurrence

256
Q

what is a choriocarcinoma

A

malignancies associated with pregnancy

majority follow trophoblastic moles, but can also follow normal pregnancy

1/20 000 pregnancies

257
Q

risk factors for choriocarcinoma

A

same as molar pregnancy

type A women with type O men

258
Q

symptoms of choriocarcinoma

A

abnormal bleeding after any pregnancy

259
Q

treatment for choriocarcinoma

A

chemo–> methotrexate, cyclophosphamide/vincristine, etoposide/actinomycin D/MTX

D and C

260
Q

list the types of contraception

A

rhythm

coitus interruptus

lactational amenorrhea

barrier

IUD

norplant

depoprovera

vasectomy

tubal sterilization

OCP

261
Q

what is the rhythm method of contraception

A

fertility awareness/abstinences

55-80% effective

ovulation assessment–> BBT

menstrual cycle tracking

cervical mucus exam

262
Q

what is the coitus interruptus method of contraception

A

withdrawal before ejaculation

15-25% failure

263
Q

what is the lactational amenorrhea method of contraception

A

nursing delays ovulation by hypothalamic suppression

maximum of 6 months

50% ovulate by 6-12 months

15-55% get pregnant while nursing if no other method

264
Q

what are the barrier methods of contraception

A

male and female condom

diaphragm

cervical cap or sponge

spermacide

265
Q

how does the copper IUD work

A

spermicidal response/inhibition of implantation

used when OCP contraindicated and patient is a low STD risk

contraindicated in pregnancy, abnormal vag bleeding, infection

relative contraindication–> nullip, prior ectopic, history of STD, moderate or severe dysmenorrhea

266
Q

failure rate of copper IUD

A

less than 2%

267
Q

what is depoprovera

A

medoxyprogesterone acetate

IM slow release over 3 mo

0.3% failure rate

side effects–> irregular menstrual bleeding, depression, weight gain

more than 70% get irregular menses and may eventually have amenorrhea

268
Q

how does vasectomy work for contraception

A

ligate the vas deferens

less than 1% failure rate

must use condom for 4-6 weeks until azospermia confirmed on semen analysis

70% reanastomose resulting in pregnancy 18-60% of the time

50% make anti-sperm antibodies

269
Q

what is the most used method of birth control

A

tubal sterilization

270
Q

what is the failure rate of tubal ligation

A

4%

271
Q

are there side effects of tubal sterilization

A

no

272
Q

what is the risk of ectopics and risk of death with tubal sterilization

A

1/1500 ectopic

4/100 000 death

273
Q

what is the mechanism of OCPs

A

pulsatile release of FSH an LH suppresses ovulation

change in cervical mucus

change in endometrium

274
Q

what are the types of OCP

A

monophasic–> fixed dose of estrogen and progesterone

multiphasic–> varies progesterone dose each week and lower overall hormones

progesterone–> progestin only, not as effective as combo

275
Q

what are the complications of the OCP

A

thromboembolism (do not give in women with family history of DVT or PE, with PE themselves, CVA, MI, HTN

276
Q

what are some meds that decrease the efficacy of OCPs

A

PCN

tetracycline

rifampin

ibuprofen

dilantin

barbituates

sulfonamide

277
Q

OCPs cause decreased efficacy of which meds?

A

folates

anticoagulants

insulin

methyldopa

phenothiazine

278
Q

what are some benefits of the OCP

A

decrease ovarian/endometrial cancer (by 50%!!!)

decreases ectopics, anemia, PID, cysts, benign breast disease and osteoporosis

279
Q

what % of pregnancies end in therapeutic abortion

A

25%

280
Q

define the two phases of the menstrual cycle

A

follicular and luteal phases

proliferative and secretory phases

281
Q

what happens during the follicular phase of the menstrual cycle

A

release of FSH from pituitary gland results in development of primary ovarian follicle

ovarian follicle produces estrogen –> causes uterine lining to proliferate

at day 14, LH spike in response to this estrogen spike stimulates ovulation and release of ovum from follicle

282
Q

what happens during the luteal phase of the menstrual cycle

A

begins after ovulation

remnants of the follicle left behind in the ovary develop into the corpus luteum –> secretes progesterone which maintains endometrial lining in prep for implantation if ovum is fertilized

if no fertilizations, corpus luteum degenerates and progesterone levels fall

without progesterone, endometrial lining is sloughed off–> menstruation

283
Q

what effect does the progesterone produced by the corpus luteum have on the endomterial lining

A

becomes thicker, more glandular and secretory

if fertilization occurs, trophoblast produces hCG which acts to maintain the corpus luteum so it can continue to produce progesterone and estrogen until 8-10 weeks GA when placenta takes over

284
Q

examples of outflow tract abnormalities causing primary amenorrhea

A

imperforate hymen

transverse vaginal septum

vaginal atresia

vaginal agenesis

testicular feminization

uterine agenesis with vaginal dysgenesis

MRKH syndrome

285
Q

examples of end organ disorders causing primary amenorrhea

A

ovarian agenesis

gonadal dysgenesis 46XX

Swyer Syndrome/gonadal agenesis 46 XY

ovarian failure

enzymatic defects leading to decreased steroid hormones

Savage Syndrome–ovary fails to respond to FSH and LH

Turner’s (due to rapid atresia)

286
Q

what is Savage syndrome

A

ovary fails to respond to FSH and LH causing primary amenorrhea

receptor defect

287
Q

what is Swyer syndtome

A

gonadal agenesis with 46 XY karyotype–> testes never develop therefore no MIF therefore have both internal and external female genitalia BUT no estrogen so no breasts

cause of primary amenorrhea

288
Q

central disorders causing primary amenorrhea

A

hypothalamic

local tumour compression

trauma

TB

sarcoidosis

irradation

Kallman syndtome (congenital absence of GnRH)

pituitary problems

damage from surgery or radiation therapy

hemosiderosis deposition of iron in the pituitary

289
Q

where is GnRH produced

A

hypothalamus

290
Q

in the presenting complaint of primary amenorrhea, what should you think of if the patient also has:

absent breasts
absent uterus

A

gonadal agenesis in 46 XY

291
Q

in the presenting complaint of primary amenorrhea, what should you think of if the patient also has:

absent breasts with present uterus

A

gonadal failure or agenesis in 46XX

292
Q

in the presenting complaint of primary amenorrhea, what should you think of if the patient also has:

breasts present but uterus absent

A

enzyme deficiencies in testosterone synthesis

testicular feminization

Mullerian agenesis or MRKH

293
Q

in the presenting complaint of primary amenorrhea, what should you think of if the patient also has:

in the presenting complaint of primary amenorrhea, what should you think of if the patient also has:

breasts present and uterus present

A

disruption of hypothalamic-pituitary axis

hypothalamic, pituitary or ovarian pathogenesis similar to that of secondary amenorrhea

congenital abnormality of the genital tract

294
Q

how should you approach diagnosis/testing of a patient with primary amenorrhea

A

is there a uterus?

if no–> do karyotype

if yes–>

is there a patent vagina?

if no–> imperforate hymen, transverse vaginal septum or vaginal agenesis–surgery

if yes–>

are there breasts?

if no–> consider as if the progesterone challenge was negative

if yes–> progesterone challenge

295
Q

how do you approach the results to a progesterone test for secondary amenorrhea (and some primary amenorrhea)

A
  1. test is NEGATIVE–>

rule out Asherman’s syndrome and cervical stenosis

then do FSH

FSH above 40 mIU/mL–> ovarian failure

FSH below 40 mIU/mL–> severe hypothalamic dysfunction

  1. test is POSITIVE–>

are they hirsute?–> if so, consider PCOS, r/o ovarian or adrenal tumour

not hirsute–> mild hypothalamic dysfunction

296
Q

what is Asherman’s syndrome

A

cause of secondary amenorrhea

presence of intrauterine synechiae or adhesions, usually secondary to surgery to infection

297
Q

what are some things that cause hypogonadotropic hypogonadism (secondary amenorrhea)

A 
1. hypothalamic dysfunction:
kallmann
hypothalamus tumours
constitutional delay
severe hypothalamic dysfunction
anorexia nervosa
severe weight loss
severe stress
exercise 
2. pituitary disorder:
sheehan syndrome
panhypopituitarism
isolated gonadotropin deficiency
hemosiderosis (ie from thalassemia major)

Obstetrics and Gynecology (21 decks)

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