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Women's Health > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

physiological consequences of ovarian failure

A
  1. vasomotor symptoms
  2. menstraul changes
  3. Sleep distrubances
  4. mood changes
  5. genital atrophy
  6. cardiovascular disease
  7. osteoporosis
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2
Q

cessation of menses for 6 months

A

menopause

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3
Q

average age of menopause

A
  1. 4

* 2 yrs earlier if a smoker and earlier if undernourished

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4
Q

late menopause-age _____

premature ovarian failure- age ____

A

late- age 50

premature- 40

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5
Q

amenorrhea, symptoms of estrogen deficiency, gonadotrophin (FSH/LH) in the menopause range

A

premature ovarian failure

*failure does not imply total cessation –> 5-10% have been able to conceive and deliver normal pregnancies because they may intermittently produce estrogen.

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6
Q

symptoms:
hot flashes
vaginal dryness
dyspareunia

A

premature ovarian failure

*normal puberty, and regulr menses prior

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7
Q

what labs do u check for premature ovarian failure

A

HCG (pregnancy)
prolactin
FSH
E2
additional labs: TSH, DEXA-scan, karyotype, auto-antibodies
*pelvic u/s and biopsy have no proven benefit

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8
Q

implications of premature ovarian failure

A
  1. osteoporosis
  2. CHD
  3. hot flashes
  4. vaginal dryness
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9
Q

treatment of premature ovarian failure

A

estrogen therapy/OCPs

*used to prevent complications of low estrogen state

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10
Q

what menopause stage?
cycle irregularity –> increased FSH, normal/high estradiol secretion (increased aromatase activity), low luteal progesterone secretion

A

early menopause

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11
Q

what menopause stage?

increased cycle variability, FSH and estradiol levels fluctuate

A

late menopause

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12
Q

what menopause stage?
no estrogen secretion by ovary; LH continues to be released which causes the ovary to continue to produce and secrete androgens

A

postmenopause

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13
Q

what is typically the 1st symptom in perimenopause/menopause

A

hot flashes/power surge

*75% of women affected

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14
Q 
symptoms:
sleep disturbance
anovulatory bleeding irregular bleeding
UTI, incontinence
sexual dysfucntion
forgetfulness, irritability
joint pain, dry skin, breast pain, migraines
A

perimenopause/menopause

*sometimes heavy bleeding during perimenopause

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15
Q

How do you diagnose menopause?

A
  • based on symptoms and mesnstrual cycle history

* 6 months of amenorrhea in a woman >45 yrs. w/ no biologic or physiologic cause (labs not routinely indicated: FSH/LH)

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16
Q

DDX of menopause

A

DDX: hyperthyroidism, pregnancy, hyperprolactinemia, medications (IUDs, chemo, radiation)

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17
Q

Increased FSH, variable cycle lengths, cessation of menstruation

A

menopausal transition

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18
Q

describe what causes menopause

A

Declining ovarian response to FSH results in decreased estrogen–> no feedback to cause an LH surge–>therefore no ovulation, no progesterone from corpus luteum, no progesterone drop off and no bleeding

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19
Q

why is there GU symptoms for menopause

A

due to less estrogen –> vaginal and urethral atrophy –> stress and urge incontinence from atrophic urethral changes and disrupted urethral seal, vaginal dryness, increased pH leading to increased vaginitis

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20
Q

why is there sexual dysfunction with menopause

A

decrease estrogen –> decreased blood flow to vagina and vulva

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21
Q

why are there skin/nails symptoms with menopause

A

increased testosterone leads to facial hair, skin is less elastic, nails become thin

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22
Q

what is the most common age group of abortions

A

45-50y/o and 14-18 y/o

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23
Q

risks associated with HRT

A
  1. thromboembolism (mostly in women with risk, E+P only)
  2. increased risk of Breast CA ( E +P only)
  3. increased risk of CHD (E+P only)
  4. increased risk of stroke (greater with E)
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24
Q

HRT has shown to be beneficial for what?

A

menopause/perimenopause

osteoporosis

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25
Q

how do you treat menopause

A

HRT

-low dose OCP (sadfe in non-smokes

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26
Q

alternative treatment options for menopause

A
  1. vaginal lubricants (replens)
  2. SSRIs/SNRIs
  3. gabapentin
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27
Q

recommendations for HRT in menopausal women

A
  1. short term therapy (2-3 yr but not more than 5 yrs)
  2. use lowest dose possible
  3. tailor to paitent’s needs
  4. women wit ha uterus need combination estrogen and progetin therapy
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28
Q

HRT for menopause is contraindicated in who?

A
  1. Hx of breast CA/ovarian CA (R)
  2. CAD (absolute)
  3. Previous venous thromboembolism or stroke (absolute)
  4. undiagnosed vaginal bleeding (absolute)
  5. pregnancy (absolute)
  6. severe liver disease (absolute)
  7. acitve gallbaldder disease (R)
  8. migraine HA (R)
  9. atypical ductal hyperplasia of the breast (R)
  10. MUST use a progestin with estrogen in women with a uterus (Estrogen-only if previous hysterectomy)**
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29
Q

___% of women have incontinence

—% of women in US have prolapse

A

20-40% of women in mid-life and beyond have some incontinence
16% have prolapse

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30
Q

why is prolapse more common in older women?

A 
more childbirths
#1 risk factor for UI is childbirth
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31
Q

cystocele

A

bladder prolapse

*most common

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32
Q

apex prolapse

A

vaginal prolapse

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33
Q

rectocele

A

retum prolapse

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34
Q

what is a prolapse?

A

hernia= tissue weakness, and a different organ falls into the bladder

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35
Q

“splint”

A

needing to enter a finger in the vagina in order to fully empty the rectum/stool in a rectocele

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36
Q

how do you exam for a prolapse

A
  1. have pt. bare down or valsalva

2. do a split sepculum exam (Isolate and look at the front and back wall of the vagina)

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37
Q

treatments for prolapse

A
  1. nothing- not life threatening but is uncomfortable
  2. pelvic floor physical therapy
    (Strengthen levator ani muscles with kegels)
  3. Pessary
  4. Surgery
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38
Q

what is the gold standard treatment for prolaspse

A

abdominal sacral colpopexy
(The upper vaginal vault is secured to the sacrospinous ligament with sutures, restoring vaginal wall support and correcting prolapse)

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39
Q

how do you repair a rectocele

A

suture based

pull healthy tissue to create a shelf

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40
Q

what is a normal amount to void urine

A

daytime: no more than once every 2 hrs (8-12x/day)
nighttime: 1-2x

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41
Q

nocturia

A

voiding more than 2x at night

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42
Q

complications of nocturia

A

sleep loss–> depression

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43
Q

available assessments for UI

A
  1. history and physical (POP-Q)
  2. Voiding diary
  3. Post-void residual
  4. Urine culture
  5. Stress test
  6. Q-tip test
  7. Uroflow
  8. Urodynamics
  9. Cystoscopy
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44
Q 
cough
sneeze
laugh
exercise
position change
A

stress UI

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45
Q

urgency
frequency
nocturia
dysuria

A

urge UI

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46
Q

hesitancy
interrupted flow
poor stream
incomplete void

A

overflow UI

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47
Q

hypermobile urethra

A

stress UI

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48
Q

detroucer mm. contracts too frequently “I know every bathroom in town”

A

urgency UI

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49
Q

UI caused by neurologic injury or DM

A

overflow UI

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50
Q

sections in a voiding diary

A 
3 day diary
intake
output
frequency
activities associated w/ incontinence
insensible loss
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51
Q

what do you check for on PE when evaluating for UI

A
  1. estrogen status
  2. Neuro screening (bulbocavernosus and anal wink reflexes)
  3. Anatomical defects resting and straining (POP-Q)
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52
Q

what nerves affect UI

A

S2, 3, 4 keeps your pee pee off the floor

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53
Q

Test that evaulate for UI

A
  1. CST (cough stress test)
  2. Postvoid residual (PVR)
  3. Multichannel Urodynamics (UDS)
    * don’t do Q-tip test (no predictive outcome)
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54
Q

definitely abnormal PVR

A

> 200cc

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55
Q

what is the Q-tip test suppose to detect

A

urethral hypermobility

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56
Q
  • Uses instruments to measure and display physiologic functions of lower urinary tract
  • Pressure catheter in bladder and vagina or rectum
  • Pdet calculated
A

Multichannel Urodynamics (UDS)

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57
Q

indications for Multichannel Urodynamics (UDS)

A
  1. Uncertain diagnosis (Findings don’t match complaint)
  2. Complex history
  3. Previous surgery
  4. Patient not satisfied with initial treatment
  5. Surgery planned in a complicated patient
  6. Comorbid conditions
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58
Q

treatments for UI

A 
Nonsurgical:
pelvic floor muscle training
bladder training
prompted voiding
lifestyle modifications
anticholinergic drugs
Surgical:
open retropubic colposuspension (burch procedure)
Sling procedure
Sacral neuromodulation
Botox
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59
Q

what lifestyle modifications can you do to help with UI

A
  1. restrict fluid intake
  2. avoid caffeine and alcohol
  3. Minimze evening intake of fluids (quit drink 2 hrs before bed)
  4. manage constipation
  5. smoking cessation
  6. treat pulmonary disease
    * other irritants: white wine, vit. C, artificial sweetner
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60
Q

Frequent voluntary voiding to keep the bladder volume low

A

bladder training

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61
Q
  • Bladder filling begins with an audible signal to let the patient know the bladder pressure is rising; tone varies with increasing pressure; bladder is repeatedly filled while patient focuses on suppressing detrusor contractions
  • 1 hour session per week
A

biofeedback

*also used for pelvic floor strengthening exercise

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62
Q

Mainstay of medical treatment for overactive bladder

A

anticholinergic drugs

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63
Q

how do anticholinergic drugs help UI

A

prevents spasming of the bladder

*may cause dry mouth, eyes and consipation

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64
Q

Most commonly prescribed anticholinergic drugs

A

Oxybutinin (Ditropan)
Tolteridine (Detrol or Toviaz)

*typically takes 2-3 tries before finding one that works

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65
Q

sacral neuromodulation

A

“pacemaker” to the bladder to treat UI
(Minimally invasive, Minimal pain, Fluoroscopy, Simple technique)

-reversible

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66
Q

how does botox help UI

A

prevents bladder spasm

*need repeat shot every 6 months

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67
Q

how many kegels should you do

A

30 each day with 10sec squeezing: 10 sec rest

68
Q

first-line of treatment of USI

A

kegels

69
Q

1st line of therapy for prolapse

A

pessaries (supportive donut-like ring that go behind pubic bone)

70
Q
  • Collagen, carbon-coated beads, fat
  • Periurethral/transurethral Injection around bladder neck and proximal urethra
  • “Washer effect”
A

Periurethral bulking agents

71
Q

proposes that urinary incontinence results from a failure of the pubourethral ligaments in the mid-urethra, therefore treat with

A

therefore use tension-free vaginal tape

72
Q

placed at the miduretrha to raise the urethra back into place – can be performed vaginally

A

TFT

*likely new gold standard

73
Q

refer to urogyn when?

A
  • Symptoms do not respond to initial treatment within 2 to 3 months
  • recurrent symptomatic UTI
74
Q

dimpling or pulling of breast tissue occur when what is affected?

A

Cooper’s ligament

75
Q

how often do you perform a breast exam

A

1-3 yrs for women 20-39
annually if >40
*encourage breast awareness exams

76
Q

how do u describe the location of a breast lump

A

use a clock-like description (3 oclock, 2cm from nipple)

77
Q

women start having a mammogram yearly at what age

A

40

  • in a pt with 1st degree relative w/ early onset of breast CA, start screening 10 yrs prior to relatives dx
    (ex. mom dx at 45, start mammogram at 35)
  • *could get false + if done too early
78
Q

mammogram screening vs 3D (digital breast tomosynthesis)

A
  • 3D allows for multiple view (screening has 2 views)
  • 3D better for women with dense breast
  • 3D has 8% more radiation
79
Q

BI-RADS

A

breast imaging reportin and data system

1 inadequate pic, 2 neg—> 6 known bipsy-proven

80
Q

why are breast u/s useful

A

differentiating between cystic and solid

81
Q

when are breast MRIs recommended

A

for women with >20% CA risk

*not good for screening bc a lot of false positives are picked up (high sensitivity, low specificity)

82
Q

describe a malginant lump

A

poorly defined
usually less mobile
non-tender
may cause skin dimpling or nipple retraction
may have nipple discharge
may have overlying skin changes (pea d’ orange)

83
Q

how do u further assess a palpable lump

A
  1. imaging

2. breast biospys (incisional or excisional) vs core-needle biospy or FNA

84
Q

obtains clusters of epithelial cells

  • interprets as bengin or mallignant
  • higher insufficient sample rate
A

FNA

85
Q

vacuum-assisted device that removes multiple cores of tissue

A

core needle

86
Q

triple test

A

clinical exam
imaging
needle biopsy
*99% accurate when all 2 c/w benign lesion

87
Q

mastodynia or mastalgia

A

severe breast pain >5 days/month

*most common in perimenopausal women

88
Q

when is cyclic breast pain worst

A

right before menses

89
Q

tx of cyclic breast pain

A
  1. NSAIDS or tylenol
    -supportive bra
    OCPs
    limiting caffeine (not proven)
    evening primrose oil
    warm or cool compresses
90
Q

what do u want to check out with non-cyclic breast pain

A

bilateral: PRL (prolactin) and BHCG (pregnany test)

r/o musculoskeletal, cardiac, chest wall, meds, cyst, mass

91
Q

Probable hormonal influence since _______ wax and wane with the menstrual cycle,

A

fibrocytic changes

  • becoming more palpable (and tender) just prior to menses
  • not a disease
92
Q

how do u dx breast simple cysts

A

u/s

sonolucent, smooth margins

93
Q

how to tx breast simple cysts

A
  • often go away on own or fluctuate w/ menstrual cycle
  • can be aspirated if symptomatic
  • can excise if recurrent
94
Q

May see septations or intracystic masses

Wall thickening or irregularity

A

complex cyst

*require excision or biopsy

95
Q

Benign, focal abnormality of a breast lobule

A

fibroadenoma

96
Q

Feel rubbery, firm, well-marginated, very mobile, usually painless

A

fibroadenoma

97
Q

how to f/u with fibroadenoma

A

Imaging at minimum with potential biopsy or excision

98
Q

what is the most common cause of breast infection

A

S. aureus

99
Q

Symptoms: localized swelling, erythema, pain, warmth, chills, fever, flu-like symptoms

A

Puerperal Breast Infections: mastisis

100
Q

mastisis affects ___% of nursing moms

A

2-3%

101
Q

how to treat Breast Infections: Puerperal

A

antibiotics (consider abscess if no improvment after 48 hrs)

*Continue nursing, apply heat, avoid cracked nipples

102
Q

examples of Breast Infections: Nonpuerperal

A

cellulitis

abcess

103
Q

olliculitis, infection of epidermal inclusion cysts

A

peripheral abcess

104
Q

how do u tx an abcess

A

antibiotics or incision and drainage (I and D)

105
Q

how do u tx cellulits

A

antibiotics

*Uncommon, should prompt imaging if unresolved

106
Q

arise from keratin-plugged milk ducts

A

subareolar abcess

107
Q

how do u tx subareolar abcess

A

incision and drainage or duct excision

108
Q

Mastitis Treatment

A 
Course of abx for 7 – 10 days
Cephalexin**
Amoxicillin/Clavulante
Azithromycin
Dicloxacillin**
Clindamycin
*F/U w/ documented resolution is imperative
109
Q

who expresses nipple discharge

A

40% of premenopausal women
55% of parous women
74% of women who have lactated in the last 2 yrs

110
Q

Benign Characteristics of nipple discharge

A

White, green, or yellow
NOT spontaneous (after intercourse or shower)
Bilateral

111
Q

pathologic characteristics of nipple discharge

A

Unilateral or single duct
Spontaneous
Persistent
Bloody/red, pink, orange, brown, black, or clear

112
Q

causes of nipple discharge

A

Physiologic (Manual stimulation, traum)
Pathologic (Galactorrhea, prolactinomas, primary hypothyroidism)
-Pharmacologic (Psychoactive and antihypertensive agents, opiates, marijuana, estrogen-containing meds)
- Idiopathic

113
Q

Gynecomastia

A

Literally means “female breasts”

Men may have visible enlargement of breast or palpable change (often feels like a firm, rubbery subareolar mass)

114
Q

cause of Gynecomastia

A
  • Results from excess estrogen or estrogen/testosterone imbalance
  • Symptom of physiological change, drug side effect (drugs that increase estrogen level), other disease, tumor, idiopathic
  • Prevalence increases with age
115
Q

Pathophysiological causes of gynecomastia

A

hypogonadism, hyper/hypo-thyroidism, ETOH-induced liver cirrhosis, testicular tumors, adrenal tumors

116
Q

what is the prevalence of breast CA

A

1: 8
* Women are 6 times more likely to die from heart disease
* risk increases w/ age (median age 61)
* incidence is highest in white women but mortalitiy is higher in AA

117
Q

most common CA in women

A

breast cancer > colorectal > lung

118
Q

factors that increase ones risk of breast CA

A
  1. female
  2. age
  3. genes (BRCA1/2)
  4. Fhx
  5. PMH
  6. high breast tissue density
  7. high-dose radiation to chest
  8. never breastfed, no full term pregnancies, recent OCP use
  9. alcohol
  10. height
119
Q

estimates a woman’s risk of developing invasive breast CA over the next 5 yrs and in their lifetime (up to 90)
uses 7 risk factors
history of LCIS or DCIS
age
age at onset of menstration
age at the time of their first live birth
number of 1st degree relatives wiht breast CA
history of breast biopsy
race/ethnicity

A

Gail Model

120
Q

When do u consider prophylatic Breast CA therapy for a woman?

A

5 year risk of > 1.7% according to Gail model
consider chemoprevention with tamoxifen/raloxifene (decreases rate of invasive breast cancer by 50% after 5 years of treatment)

121
Q

> 20% lifetime risk: consider annual mammography plus breast MRI, CBE every 6 mo., monthly BSE

A

tyrer-cuzik model = adds in famililal risk

122
Q

True or False?

Most cases of
breast cancer are
a result of
inherited genetic
mutations
A

false

*Genetic mutations likely account for between 5 and 10% of breast cancers

123
Q

what types of genes are BRCA 1/2

A

tumor suppressor genes

*Accounts for 3 – 5 % of breast cancers (10% of ovarian cancers)

124
Q

Chromosome 17
More common
More aggressive tumors  grade III, Her2/neu and ER-negative
More risk of ovarian CA (39 – 46%)

A

BRCA 1

125
Q

Chromosome 13
Responsible for the majority of male breast cancers
Carries increased risk for pancreatic, prostate, and stomach CA, and melanoma
Risk of ovarian CA 12 - 20%

A

BRCA 2

126
Q

screenig when BRCA +

A
  • CBE twice a year + annual mammography and MRI beginning at age 25 years (or sooner based on earliest age onset in the family)
  • “Periodic” CA 125 and transvaginal US starting at 30 yo (or 5 – 10 years before age of first ovarian CA diagnosis)
127
Q

treatment for BRCA +

A
  • Bilateral mastectomy reduces the risk of breast cancer by 90–95%
  • BSO by age 40 years (or after childbearing) reduces ovarian cancer risk by 85–90% and breast cancer risk by 40 – 70%
  • Tamoxifen reduces breast cancer risk by up to 62% in BRCA2 patients
128
Q

different types of breast CA

A

Ductal carcinoma
(most common)
Lobular carcinoma
Other types

DCIS
LCIS
*non-invasive CA, well localized

129
Q

Originates in the cells lining the milk ducts

> 80% of all breast cancers are this type

A

invasive ductal carcinoma

130
Q

10-15% of all breast cancers

Originates in the lobes of the breast

A

invasive lobular carinoma

131
Q

1-5% all breast CA
Cancer cells block lymph vessels of the skin
Quite aggressive, often occurs in younger women and more common in AA women
Peau d’orange, inflamed appearance

A

inflammatory breast CA

132
Q

Usually non-palpable and detected on mammogram
Often associated with calcifications
20% all mammographically detected cancers

A

DCIS (ductal carcinoma in situ)

*Risk of progression to invasive cancer is unknown

133
Q

treatment of DCIS

A

lumpectomy (+/- radiation) or mastectomy

134
Q

Incidental finding
May require surgical intervention
Most helpful as marker for increased risk (20-30%) for invasive breast ca in either breast

A

LCIS (Lobular carcinoma in situ)

135
Q

breast CA Prognostic Factors

A 
Size: the smaller, the better
Grade: differentiation and rate of proliferation
ER/PR status
Her2/neu oncogene overexpression
Lymph node (LN) involvement
136
Q

breast CA treament

A
  1. chemo
  2. surgery
  3. radiation
  4. endocrine therapy
137
Q

tx type?

Multiple regimens, often after surgery but may be pre-operative if large tumor, IV and oral agents

A

chemo

  • tx 3-6 months
  • Combination therapy best, anthracycline-containing regimens are usually best
138
Q

tx type:
Lumpectomy (can be assisted by needle localization if non-palpable), mastectomy, sentinel lymph node biopsy, axillary dissection

A

surgery

139
Q

____% dominant breast lesions are malignant

A

20%

140
Q

a true hernia at the top of the vagina allowing the small bowel to herniate though

A

enterocele

141
Q 
what POP-Q stage?
no prolapse( (the the cervix is at least as high  as the vaginal length)
A

stage 0

142
Q

what POP-Q stage?

leading edge is more than 1 cm beyond the hymen, but less than or equal to the total vaginal length

A

stage 3

143
Q

what POP-Q stage?

complete eversion

A

stage 4

144
Q

what POP-Q stage?

Leading part of prolapse is more than 1 cm above the hymen

A

stage 1

145
Q

what POP-Q stage?

leading edge is less than or equal to 1 cm above or below the hymen

A

stage 2

146
Q

Procidentia

A

when the cervix descends beyond the vulva

147
Q

a clear or milky breast discharge is usually bilateral and associated w/ stimulation or elevated prolactin levels

A

galactorrhea

148
Q

bilateral salpingo-oophorectomy

A

removal of fallopian tubes and ovaries

149
Q

intraductal growths composed of abundant stroma and lined by both luminal and myoepithelial cells

A

papillomas

150
Q

Polythelia

A

extra nipples

151
Q

Polymastia

A

extra breasts

152
Q

an increase in the number of glands with associated lobular growth

A

adenosis

153
Q

more than 2 cell layers on basement membrane

A

Epithelial Hyperplasia

154
Q

increased fibrosis within the expanded lobule with distortion and compression of the epithelium

A

Sclerosing Adenosis

155
Q
  • a nidus of tubules entrapped in a densely hyalinized stroma surrounded by radiating arms of epithelium
  • mimic an invasive carinoma
A

Radial Scar-

156
Q
  • intraductal growths composed of abundant stroma and lined by both luminal and myoepithelial cells
A

Papillomas

157
Q

obliteration of the lumina of the glandular acini by a uniform population of small, atypical cells
*relaed to atypical lobular hyperplasia

A

LCIS

*tx w/ excisional biopsy

158
Q

the ducts are filled with atypical epithelial cells

A

DCIS

*evaluate with core needle biopsy followed by surgical biopsy or excision

159
Q

5-15% of all breast CA

often multifocal and bilateral

A

invasive lobular carcinoma

160
Q

70-80% of all breast CA

most likely to spread to lymph nodes

A

invasive ductal carcinoma

161
Q

stage breast CA based on what system

A

TNM

tumor size, involvment of lymph nodes, and distant metastasis

162
Q

used in the treatment of all stages of breast CA, regardless of lymph node status
-Includes chemotherapeutic drugs that kill CA cells and hormonal therapies such as tamoxifen that act as estrogen antagonists

A

adjuvant (systemic) medical therapy

163
Q

prevent the production of estrogen in postmenopausal women
used to extend survival in women with metastatic CA, as a primary adjuvant therapy, an din conjunction with tamoxifen to prevent CA recurrence

A

aromaste inhibitors (AIs)

164
Q

-acts on membrane-bound protein produced by Her2/neu

0if a pt’s CA is found to overexpress Her2/neu protein,_____ can be given as adjuvant therapy

A

trastuzumab

165
Q

f/u after breast CA treatment

A
  • OB/gyn screens for the first 2 years (f/u every 3-6 months and then annually after that)
  • annual mammography and PE continue indefinitely after that
166
Q

what percentage of breast CA are due a BRCA + gene?

A

3-5%

167
Q

what percentage of ovarian CA are due to BRCA + genes?

A

10%

Women's Health (3 decks)

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