Final Exam Flashcards
(150 cards)
1
Q
Primary Amenorrhea vs Secondary Amenorrhea
A
Primary- no menarche by age 16
-evaluation if no menarche by 15 or within 3 years of thelarche (breast development); no breast development by age 13
Secondary- lack of menstruation for 3-6 months or the length of 3 menstrual cycles
2
Q
Amenorrhea Causes
A
pregnancy
hypothalamic-pituitary dysfunction
ovarian dysfunction
genital outflow alterations
3
Q
Evaluation for primary amenorrhea
A
history and physical
lab tests- HCG. FSH, TSH, PRL, possibly LH
Pelvic ultrasound
4
Q
Primary Amenorrhea evaluation
A
breast development
presence or absence of uterus
FSH levels
5
Q
Most important step in amenorrhea workup
A
determine by physical exam or ultrasonography if there are any anatomic abnormalities of the vagina, cervix, or uterus
6
Q
elevated FSH level in amenorrhea
A
probably diagnosis is gonadal dysgenesis
karyotype should be obtained
7
Q
If the uterus is absent and FSH is normal in amenorrhea
A
probable diagnosis is Mullerian agenesis or androgen insensitivity syndrome (circulating testosterone is in the male range)
8
Q
If FSH is normal and breast development is present but imaging detects accumulated blood in uterus (hematometra) or vagina (hematocolpos) in amenorrhea
A
obstructed outflow tract present
9
Q
If FSH is low or normal but uterus is present in amenorrhea
A
workup for degree of pubertal development
distinguish between constitutional delay of puberty and congenital GnRH deficiency
also investigate possible causes of secondary amenorrhea
10
Q
Initial evaluation for secondary amenorrhea
A
history and physical
Initial labs: HCG, FSH, TSH, PRL, E2, Total T
11
Q
If pregnancy test is negative in secondary amenorrhea…
A
evaluate if the patient has adequate estrogen, a competent endometrium, and a patent outflow tract
do Progesterone Challenge Test
12
Q
Progesterone Challenge Test
A
Medroxyprogesterone acetate or micronized progesterone given for 10-14 days and is expected to induce withdrawal bleeding within a week of the test
13
Q
If bleeding occurs after Progesterone challenge
A
sufficient estrogen, presumed anovulatory (extra-ovarian sources)
14
Q
If bleeding does not occur after progesterone challenge
A
patient may be hypoestrogenic or have an anatomic condition or obstruction
15
Q
High serum prolactin concentration in secondary amenorrhea
A
can be increased by stress ore eating
measure at least twice before ordering cranial imaging
screen for thyroid disease- hypothyroidism can cause hyperprolactinemia
refer to endocrinology
16
Q
High serum FSH concentration in secondary amenorrhea
A
indicates primary hypogonadism (ovarian failure or insufficiency)
17
Q
Normal or low serum FSH concentration in secondary amenorrhea
A
indicates secondary hypogonadism (PCOS or hypothalamic amenorrhea)
18
Q
High serum androgen concentration in secondary amenorrhea
A
depending on clinical picture can solidify PCOS diagnosis or may raise question of androgen-secreting tumor of ovary or adrenal gland
refer to endocrinology
19
Q
Treatment of secondary amenorrhea
A
directed at correcting the underlying pathology
achieve fertility if desired
prevent complications of the disease process
20
Q
Treatment of hypothalamic causes of amenorrhea
A
seen in many athletic women
education on adequate caloric intake and decreased exercise
referrals as appropriate
CBT
management of low bone density
21
Q
Treatment of hyperprolactinemia in amenorrhea
A
treatment depends on cause and patient goals
treated by endocrinologist
22
Q
Treatment of primary ovarian insufficiency in amenorrhea
A
postmenopausal hormonal therapy for prevention of bone loss
oral contraceptives (intermittent ovarian function)
replacement of estrogen and/or progestin
23
Q
Treatment of hyperandrogenism in secondary amenorrhea
A
directed toward achieving women’s goal
relief of hirsutism
resumption of menses
fertility
preventing long-term consequences of PCOS
endometrial hyperplasia
obesity
24
Q
Abnormal uterine bleeding
A
majority of cases are just after menarche or perimenopausal period
most cases related pregnancy, structural uterine pathology (fibroids, polyps, adenomyosis)
anovulation
neoplasia
25
Evaluation of abnormal uterine bleeding
Frequency: normal 24-38 days
Regularity: between cycles, 7-9 days: depending on age
Duration: normal <8 days
Volume: subjective, normal does not interfere with a patients quality of life
26
Evaluation of AUB
Frequency: normal is 24-38 days
Regularity: between cycles depending on age: 7-9 days
Duration: normal <8 days
Volume: subjective. normal does not interfere with a patient's quality of life
27
Most common cause of amenorrhea
pregnancy
28
Abnormal uterine bleeding causes
failure to ovulate (?)
anovulatory causes- PCOS, obesity, adrenal hyperplasia
Ovulatory causes- typically cyclic; usually anatomic or physical lesion *heavy or prolonged bleeding*
-fibroids
-adenomyosis
-polyps
-uterine malformation
29
Chronic estrogen production unopposed by adequate progesterone production
allows for the continued proliferation of the endometrium
thickened endometrium outgrows its blood supply and undergoes focal necrosis with partial shedding
bleeding is usually irregular, prolonged, and heavy
30
Initial evaluation of AUB
history: medical, gyn/OB, menstrual, sexual, cancer
physical exam
pregnancy test
labs: CBC, cervical Ca screening, STIs
31
In the first decade after menarche...
HPO axis is immature and may not ovulate each month.. leading to irregular bleeding
32
Who is most likely to have benign and malignant growths?
women between the age of 40 and menopause
33
Heavy menstrual bleeding evaluation
Imaging to r/o fibroids, adenomyosis, polyps, malformations
Labs: normal plus ferritin, clotting factors, TSh
Endometrial sampling: hyperplasia or malignancy
34
Intermenstrual bleeding evaluation
spotting or bleeding throughout month
imaging to r/o polyps scars or defects
Endometrial sampling concern for malignancy
35
Irregular bleeding evaluation
usually ovulatory dysfunction
imaging to r/o polyps scars or defects
labs: TSH, PRL, Androgens, FSH, E2
Endometrial sampling if symptoms occur >6 months for hyperplasia or malignancy
36
Treatment of AUB
ensure regular shedding of endometrium and bleeding
use of progesterone for 7-10 days to stimulate withdrawal bleeding
use of COCs to regulate bleeding patterns
endometrial ablation if other treatments are ineffective with no future childbearing
37
Premenstral syndrome
physical and behavioral symptoms that occur in the second half of menstrual cycle (luteal phase)
abdominal bloating
breast tenderness
HA
edema
anxiety
depression
confusion
social withdrawal
angry outburst
38
Premenstral dysphoric disorder
affects 3-5% of women outlined in DSM-5 criteria
at least 5 or more symptoms are present in week before menses and resolve in days following menses
distinguish from depression, anxiety, or hypothyroidism
detailed history
if a woman DOES NOT a symptom-free interval they do not have PMS/PMDD
39
mild to moderate PMS treatment
directed toward specific symptoms
encourage physical acticity
dietary modification- limit caffeine
use of calcium and magnesium supplements
herbal products
therapy, biofeedback, acupuncture, reflexology, relaxation therapy
COC use- continuous use?
40
PMDD first line treatment
SSRI- fluoxetine, sertraline, paroxetine
if one is not successful, try another!
hormonal therapy
progestin-based contraceptives- DMPA, hormonal IUDs
COCs- continuous use?
41
Dysmenorrhea
painful menstruation that prevents a woman from doing her normal activities
may be accompanied by diarrhea, nausea, vomiting, headache, and dizziness
42
primary vs. secondary dysmenorrhea
primary greatest in teens and early 20s- caused by excess prostaglandin F2a produced in the endometrium
secondary becomes more common as a woman ages because of increasing prevalence of causal factors; caused by structural abnormalities or disease processes that occur outside the uterus, within the uterine wall, or within the uterine cavity such as endometriosis adenomyosis, or uterine fibroids
43
Patient history with dysmenorrhea
heavy menstrual flow with pain- suggestive of adenomyosis, fibroids, polyps
feeling of pelvic heaviness or change in contour of abdomen could be large fibroid or cancer
fever, chills, malaise- signal infection
coexisting complaint of infertility may suggest endometriosis or PID
44
Primary Dysmenorrhea
caused by excess prostaglandin F2a that is produced in the endometrium; prostaglandin production increases under the influence of progesterone and peaks around menses
can cause uterine contractions with pressures than can exceed 400mmHg
baseline contraction pressure are about 80mmHg, normal baseline is 20mmHg
45
Prostaglandins
cause muscle contractions and can cause them places other than the uterus, cause N/V/D
46
Diagnosis of primary dysmenorrhea
recurrent month after months occurring in the first few days of menstruation
dyspareunia generally not found in primary dysmenorrhea
47
Prostaglandin E2
produced in uterus
potent vasodilator and inhibitor of platelet aggregation (heavy periods)
48
Secondary dysmenorrhea
caused by structural abnormalities or disease processes outside the uterus, within the uterus, or within uterine wall
endometriosis, tumors, adhesions, PID
pain lasts longer than menstrual period, may start prior to bleeding, become worse during menses, persists after menstruation ends
49
Clinical features that separate secondary from primary dysmenorrhea
enlarged uterus, pain with intercourse, resistance to effective treatments
50
Assessment for secondary dysmenorrhea
PE directed toward finding secondary cause
Pelvic- asymmetry or enlargement may suggest tumor or fibroids
Painful nodules in the posterior culdesac with restricted cervical motion may suggest endometriosis
restricted motion may also suggest scaring/inflammation
Obtain cervical cultures- GC and CT, R/O PID
Imaging
laparoscopic exam may establish final diagnosis
51
Primary dysmenorrhea should not be diagnosed without ruling out...
secondary causes
-PE should be normal in primary
52
Therapy for dysmenorrhea
vast majority with primary find relief with NSAIDs
heat
exercise
psychotherapy
COC
Reassurance
53
Therapy for secondary dysmenorrhea
severe cases may require surgical intervention
-pre sacral neurectomy
other procedures targeted toward underlying condition
54
Acute pelvic pain
lower abdominal or pelvic pain that has lasted less than 3 months
over 1/3 of reproductive aged women will experience non-menstrual pelvic pain
55
Etiologies of acute pelvic pain
PID
Tube-ovarian abscess
hemorrhage, rupture, or torsion of an ovary or ovarian neoplasm
torsion of fallopian tube
endometriosis
endometritis
dysmenorrhea
ovarian hyperstimulation syndrome
56
Differential diagnosis for acute pelvic pain
appendicitis
ovarian cyst
pyelonephritis
lower UTI
renal calculi
GI conditions
57
Acute pelvic pain with positive pregnancy test
r/o ectopic pregnancy or miscarriage
58
Visceral pain
receptors responsible for these sensations are located on serial surfaces, within the mesentery, and within the walls of hollow viscera
deep, dull, vague, poorly-defined sensation
59
Visceral pain in acute pelvic pain
distention of a viscous or organ capsule
spasm of intestinal muscularis fibers
inflammation or infection
ischemia from vascular disturbances
hemorrhage
neoplasm
60
Somatic pain
includes abdominal and pelvic muscle fascia, parietal peritoneum, subcutaneous tissue, and skeletal system
d/t myofascial trigger points
hernia
hematoma
muscle strain or injury
inflammation
trauma
pain directly over inflamed area
pain usually steady and aching in character
tension in area increases pain
will see guarding or rebound tenderness
61
Carnett sign
positive (myofascial) if pain increases on tensing of the abdomen
negative (visceral source) pain stays the same or decreases
62
Neurogenic pain
occasional d/t injury to sensory nerves
herpes zoster
impingement by arthritis or tumors
diabetes
MS
syphilis
63
Evaluation of acute pelvic pain
first priority is to identify life-threatening conditions requring emergent management
shock or peritoneal signs may require immediate surgical interventiosn
Hx: detained sexual history with normal history
Physical exam: abdominal pelvic GU
S/S: oral temp >101, abnormal vaginal discharge, presences of abundant numbers of WBCs on saline microscopy of vaginal secretions, documented chlamydia or gonorrhea
64
Follicular cyst
develops when a follicle fails to rupture during follicular maturation and ovulation does not occur
pelvic exam may reveal tender unilateral adenexa and mobile mass
rupture cause acute pain
responds to COCs
typically resolve in 6 weeks
do pelvic US
65
Corpus luteum cyst
occurs when corpus luteum fails to involute and continues to enlarge after ovulation
related to progesterone dominant phase post-ovulatory
menstration is delayed- due to prolonged progesterone secretion
pain and missed periods are most common complaints
may benefit from COCs
lots of pain
66
luteal phase cyst
ruptures late in luteal phase and includes spontaneous hemorrhage
pts usually not on OC, have regular periods
acute pain in luteal phase
some present with hemiperitoneum and hypovolemia
repetitive hemorrhagic cysts require hemodynamic investigation
67
Tubo-ovarian abscess
severe and potentially life threatening- Emergency treatment
Primary TOA:
PID, following pelvic surgery, or with ovarian hyperstimulation
Secondary TOA:
bowel perforation with intra-peritoneal spread of infection
in association with pelvic malignancy
68
Microbiology associated with TOA
mixed polymicrobial infection with high prevalence of anaerobes
common: Streptococcal, E. coli, Bacteroides fragilis, Prevotella, and Peptostreptococcus
HIV: mycobacterium tuberculosis
69
Diagnosis of TOA
should be considered in any patient suspected of PID
abdominal and/or pelvic pain are present in 90% of patients with TOA
complete history and pelvic exam
laboratory: CBC, GC/CT, HCG, may add ESR or CRP
Imaging: Pelvic ultrasound (1st line) can also use pelvic CT
fever and leukocytosis (but not in all patients)
70
Treatment of tubo-ovarian abscess
outpatient treatment is unsafe
ER for evaluation- antibiotics given to stable patients
need close monitoring
emergency surgical intervention
life threatening
71
chronic pelvic pain
non-cyclic pain that is perceived to be in the pelvic area that has persisted for six months or longer, unrelated to preganncy, and causing functional disability or leading to see medical care
72
Evaluation of chronic pelvic pain
OLDCART emphasis on timing and severity
medical, surgical, menstrual, sexual history, bowel/bladder function
home and work conditions
social and family history
depression, abuse, sleep patterns
presume organnic cause for pain
can use IPPS questionaire
PE: pelvic exam, back, abdomen, extremities
Labs: CBC, CMP, UA and culture, Genital cultures, HIV, HCG
Imaging evaluation: transvaginal US, abdominal US, CT, MRI, colonoscopy, cystoscopy, referral
Think abuse, neurologic causes after R/O organic causes
73
Level A gynecological causes of chronic pelvic pain
endometriosis
PID
gynecologic malignancies
ovarian cysts
adhesions
adenomyosis
leiomyoma
74
Level A non- gynecological causes of chronic pelvic pain
interstitial cystitis
musculoskeletal
IBS
Bladder, Colon CA
constipation
75
IBS
characterized by crampy abdominal pain, gas, bloating, chronic diarrhea and/or constipation
relieved by bowel movement or flatulence
R/O diseases of GI tract- blood tests, stool tests, xray, or endoscopy
refer to GI
76
Treatment for IBS
limiting:
caffeine
alcohol
fatty foods
lactose or gluten intolerance
use low FODMAP diets
77
Interstitial cystitis
bladder pain syndrome
chronic pelvic pain
chonic non-infectious condition
5x mor ecommon in women than men
presents as dysuria, urinary urgency, frequency, hematuria
little known about etiology and pathogenensis
78
Treatment for interstitial cystitis
hot or cold packs
fluid management less than 2L/day
avoidance of irritating food or activities
bladder training
fluid/voiding log
first line is behavior modification and self care
pelvic floor physical therapy
Pharmacologic Treatment: pentosan polysulfate sodium
amitriptyline (not FDA approved)
Intravesical therapies
79
When to refer Interstitial cystitis
hematuria
complex symptoms
incomplete bladder emptying
neurologic disorder
prior pelvic radiation or surgery
not responding to initial treatment
80
Endometriosis
presence of endometrial tissue outside the uterus
tissue repsonse to normal hormal cycles
most frequently involves:
culdesac
ovaries
fallopain tubes
uterus
broad ligament
ureters, rectovaginal septum, uterosacral ligaments
Frequently involve:
appendix, bowel bladder
Less frequently involve: surgical scars, upper ureters, brain, lungs
81
Risk factors of endometriosis
genital tract abnormalities- retrograde menstruation
early menarche before age 11-13 or late menopause
nulliparity
first degree relative with it = 7-10x more likely to develop
82
Symptoms of endometriosis
severe dysmenorrhea
pain often precedes menses
pain with defecation, urination, deep thrusting
low back pain, pain with exercise, fatigue, malaise
heavy menstrual bleeding
reason for infertility not well understood
83
Exam for endometriosis
variable baesd on size of implants
fixed, retroverted uterus
possible adnexal masses
vaginal tenderness
nodules
laparoscopy and bioposy diagnostic
84
Treatment for endometriosis
NSAIDs
contraceptive management
dandazol
GnRH agonist and antagonist
aromatase inhibitors
neuropathic pain treatment
surgical intervention for those who do not respond to medical therapy or have ovarian involvement, large lesions
85
Ectopic pregnancy
blastocysts implants anywhere other than the endometrial lining of the uterus
98% in Fallopian tube and 80% of those in ampullary segment
Rupture of ectopic pregnancy is life threatening
86
Tubal pregnancy
can result in tubal abortion (can replant in abdominal cavity), rupture, or spontaneous resolution
87
Pathophysiology of Tubal pregnancy
inflammation may predispose women
salpingitis, PID
Chlamydia
Gonorrhea
If a woman becomes pregnant with IUD in place, she has a higher risk of ectopic pregnancy
88
Classic symptoms of tubal pregnancy
amenorrhea
vaginal bleeding
pain on affected side
no constellation of symptoms is considered diagnostic
89
Ominous signs of tubal pregnancy
shoulder pain with inspiration, syncope, vertigo from hemorrhagic hypovolemia
90
Tubal pregnancy symptoms
irregular vaginal bleeding
prior to rupture clinical findings are scant and are based on lab and US results
tenderness to pelvic and abdominal region with rupture
fever is not expected (think infection if present)
adnexal mass in approx 1/3 of cases
91
Diagnosis of tubal pregnancy
serial hCG and transvaginal US are most reliable
urine pregnancy test is reliable in stable patients
92
Medical management of tubal pregnancy
Methotrexate- folic acid antagonist
inhibits DNA synthesis and cell reproduction
Candidate if hemodynamically stable, hCG <5000 or TVUS shows no fetal cardiac activity
if patient can follow up
93
Common side effects of methotrexate
nausea, vomiting, diarrhea, gastric distress
dizziness
stomatitis
94
Pre-treatment testing for methotrexate
serum hCG
transvaginal US
blood type and screen to determine the need for anti-D immune globulin
CBC, renal and liver function tests
95
Medical vs. Surgical management of ectopic preganancy
Ovarian, Interstitial, Cervical- candidates for medical or surgical management
abdominal and heterotrophic-surgical removal
96
Post care for ectopic pregnancy
avoid vaginal intercourse until hCG is undetectable
avoid pelvic examinations due to theoretical risk of tubal rupture
avoid sun exposure, vitamins containing folic acid
pain mgmt with acetaminophen
97
Abortion
expulsion of a fetus <20 weeks
98
Spontaneous abortion
occurs in the absence of intervention
incidence about 15-25% with approx. 80% occurring in the first 12 weeks
approx 50% of early spontaneous abortions are attributed to trisomy
second trimester are more likely from maternal infection/illness, abnormal implantation of placenta, or anatomical conditions
99
Infectious causes of spontaneous abortion
CT
Listeria monocytogenes
Mycoplasma hominis
Ureaplasma urelyticum
Syphilis
HIV
GBS
100
Endocrine factors causing spontaneous abortion
thyroid antibodies
Type 1 diabetes d/t hyperglycemia, maternal vascular disease, and possibly immunologic factors
maternal weight- BMI <17 or >27 pre-pregnancy
101
Environmental factors causing spontaneous abortion
Cigarette smoking
high alcohol use in first 8 weeks of pregnancy
Drug use
NSAID use around time of conception
102
Immunologic factors leading to spontaneous miscarriage
some genetic disorders of blood coagulation may increase thormbosis
103
Uterine factors leading to spontaneous abortion
large, multiple fibroids
DES exposure in utero
Asherman syndrome
104
Threatened miscarriage
bleeding without loss of tissue or fluid
combination of pain and bleeding is usually poor prognosis for continuing pregnancy
ectopic pregnancy should always be a DD of threatened abortion
no intervention if pregnancy is intact
105
Inevitable miscarriage
vaginal bleeding with gross rupture of the membranes and cervical dilation- uterine contractions that leave to expulsion of products of conception
medical mgmt or D&C
106
Incomplete abortion
cervical os opens and allows the passage of blood
prior to 10 weeks, fetus and placenta are expelled together
later-may be delivered separately
107
Complete abortion
documented pregnancy where all contents are passed
108
Missed abortion
many women have no symptoms except amenorrhea but retain a failed pregnancy
109
Treatment of spontaneous abortion
depends on type of abortion
medical or surgical intervention for incomplete, inevitable, or missed abortions
control of bleeding is priority, making sure uterus is completely evacuated
Rh Immunoglobulin
Emotional support
110
Medical management for spontaneous abortion First trimester
Up to 12 +6 weeks gestation
Mifepristone 200mg orally followed by Misoprostol 800mcg vaginally, buccally, or sublingually
after 9 weeks there is significant improvement with a repeat dose of Misoprostol 800mg
Follow up in 1-2 weeks for US to confirm complete passage of gestational sac
111
Medical management of spontaneous abortion Second Trimester
13 to 19+6 weeks gestation
Mifepristone 200mg orally 24 hours prior to misoprostol administration
misoprostol dosing is 800mcg every 3 hours until expulsion of pregnancy tissue
typically advised to undergo treatment inpatient
112
Surgical Management for Spontaneous abortion
for all gestational ages
Dilation and curettage (D&C): aspiration performed manually or with a vacuum device
May need cervical preparation prior to D&C
prophylactic antibiotics recommended
followed up in 2 weeks. may offer phone visit in 24-48 hours
113
Induced abortion
termination of pregnancy before the time of fetal viability medically or surgically
114
First trimester induced abortion
Medication- mifepristone 200mg given orally and misoprostol self administered 24-48hours after in nonclinical setting
approved for up to 70 days gestation
Surgical management- uterine aspiration commonly performed up through 14 weeks gestation
115
Second trimester induced abortion
Medication management
-may need to induce fetal demise
may need anesthesia or epidural
Mifepristone followed by misoprostol
Surgical
-D&E, suction, extraction with forceps, and curettage
cervical dilation, injection for fetal demise, anesthesia and prophylactic antibiotics
116
Possible complications to induced abortion
uterine perforation
cervical laceration
hemorrhage
infection
incomplete removal and may need repeat D&E
117
Postabortal infection signs
fetal, pain, tender uterus, bleeding
treat with antibiotics, antipyretics, and repeat D&C
Watchout for septic abortion (rarely occurs with legal abortions)
118
Postabortal syndrome
Uterus fails to remain contracted after spontaneous abortion or elective abortion
presents with cramping, bleeding, open cervix, and hematomata
119
Incontinence
involuntary leakage of urine form the bladder
when the bladder loses its support, the mobility of the urethra pulls away and detaches from the symphysis pubis
120
Prevalence of Incontinence
increases gradually during young adult life
peaks at middle age, steadily increases in the elderly
less than half of women seek care
121
Normal voiding process
urge to void occurs when the brain receives a signal from the stretch receptors in the detrusor muscle
detrusor muscle contracts
urethral sphincter relaxes- voiding is complete
122
Detrusor overactivity (urge incontinence)
uninhibited detrusor contractions that cause increased bladder pressure and urine leakage
pts have urgency and frequency
can be related to neurologic disorders, bladder abnormalities, altered microbiome, or idiopathic
123
Stress incontinence
Increased abdominal pressure is transmitted along the urethra and end-pelvic fascia maintains bladder neck stabilization
transmission of abdominal pressure reaches the bladder but does not reach the urethra d/t weakened end-pelvic fascia
bladder neck descends, bladder pressure is then elevated above intra-urethral pressure and urine is lost
patient presents with loss of urine during:
coughing, laughing, sneezing
most common in young women
124
Mixed incontinence
symptoms of both urge and stress incontinence
patients have urine leakage with coughing, laughing, sneezing, and may also have urgency and frequency because of the rise in bladder pressure
125
Overflow incontinence
bladder does not empty completely due to detrusor weakness and/or inability to contract
may be caused by outlet obstruction or neurological deficit where the patient has lost the urge to void
patient experience a continuous leakage of small amounts of urine
126
Evaluation of incontinence
History: 3IQ form, comorbid conditions
PE
Urine culture
UA
fluid intake
medications
referral to urologist for more complex
127
Lifestyle incontinence treatment options
weight loss
caffeine/alcohol reduction
fluid management
avoid/relieve constipation
stop smoking
kegel exercises
128
Medications for incontinence
work best on urge incontiennce and mixed incontinence; have limited results on stress incontinence
anticholinergics, tricyclic antidepressants, musculotropics, topical estrogens
side effects- dry mouth, constipation, tachycardia, drowsiness
consider cost, dosing schedule, patient comorbidities, and patient situation
other: botox injection
129
Surgical options for incontinence
refer to urologist
options include:
sling procedure
retro-pubic Colpo-suspension
bulking agents placed near bladder neck: collagen, beads, fat
130
Menopausal transition
occurs after reproductive years but before menopause
oocytes become increasingly resistant to FSH- plasma concentrations increase several years in advance of actual menopause
131
Hormonal hallmark of perimenopause
fluctuating estrogen levels- not low levels
testing for this is costly, repetitive and ineffective
15-40% of menstruating women in their 40s experience hot flashes due to this
132
Perimenopause
typically occurs 4 years before final menstraiton
irregular menstrual cycles,
marked hormonal fluctuations
hot flashes, sleep disturbances, mood symptoms, vaginal dryness, osteoporosis, cardiovascular lipid changes
only diagnose to explain symptoms
rule out thyroid or medication causes
133
Hot flashes
considered one of the hallmark signs of perimenopause
caused by decreased ovarian function and estrogen production
each hot fall last approx 3 minutes, intense heat in face and chest followed by chills or a cold sweat
134
Perimenopause treatment
menopausal hormonal therapy- unopposed estrogen use for women who have undergone hysterectomy and combined estrogen-progestin therapy with intact uterus who need a progestin to prevent estrogen-associated endometrial hyperplasia
primary goal is to release hot flashes and other symptoms of menopause
135
Health promotion perimenopause treatment
more challenging for women in perimenopause/menopause to lose weight due to the decreased resting metabolic weight
due to luteal phase the metabolism is increased and without this change-calories are stored as fat
promote exercise for non weight improvements such as cardiovascular health, enhance bone remodeling, and muscle strength as well as mental health wellbeing
136
Menopause
permanent cessation of menses after cessation of estrogen production for 12 consecutive months
average age 50-52 most women between 44-55
<40yo is early menopause
137
What has no effect on age of menopause
age of menarche
number of pregnancies
lactation
OCs
race
education
height
socio-economic status
138
What does effect age at menopause
genetics, lifestyle (smoking, weight), women tend to experience menopause earlier
slender women tend to experience more menopausal symptoms because their estrogen level declines faster
139
Symptoms of menopause
hot flashes, sleep disturbances, vaginal changes, skin, hair, and nail changes, osteoporosis
140
Non-pharmacological options for treatment of menopause
stop smoking, calcium supplement, vitamin D, exercise
141
Lipid changes with menopause
Total cholesterol increases
HDL decreases
LDL increases
Hormone therapy should not be offered to patients for cardioprotective effects only
142
Primary Ovarian Insufficiency
menopause before age 40- approximately 1% of women
should be suspected in women complaining of hot flashes, secondary amenorrhea, and even complaints of infertility
diagnosis is confirmed by FSH levels in the menopausal range (>30mlU/ml) on two separate occasions
causes: genetic factors, savage syndrome, autoimmune disorders
143
Causes of primary ovarian insufficiency
smoking, alkylating cancer chemotherapy, hysterectomy
144
Management of menopause
oral, transdermal, or topical estrogen
17-B estradiol
start with lowest does and titrate up
145
Endometrial cancer
develops in 1-2% of women in the US and 4th most common cancer in US women
incidence peaks between ages 60-70 years but 2-5% of cases occur before age 40
typically a disease of post-menopausal women
usually presents early with abnormal uterine bleeding (80-90% of women)
146
most common precursor to endometrial cnacer
endometrial hyperplasia
Type 1- Grade 1/2: estrogen-dependent
Type 3- Grade 3/4 estrogen- independent
poorer progosis
147
Treatment of endometrial cancer
hysterectomy is primary treatment
148
Osteoporosis risk factors
early menopause
sedentary lifestyle
smoking
low body weight
excessive alcohol consumption
149
Fracture risk assessment tool (FRAX)
normal bone mass >-1
osteopenia (low bone mass) -1 to -2.5
osteoporosis < -2.6
150
First line therapy for osteoporosis
Biphosphonates
Alendronate/ Risedronate
