M29

Sexuality and Sexual Dysfunction

SEXUAL RESPONSE

1. desire:energy that allows an individual to initiate or respond to sexualstimulation (libido)

2. arousal:physical and emotionalstimulation leading to breast and genital vasodilation and clitoral

engorgement (excitement)

3. orgasm: physical and emotionalstimulation is maximized, allowing the individual to relinquish their

sense of control

4. resolution: most of the congestion and tension resolves within seconds, complete resolution may take

up to 60 min

Note: thisframework cannot be applied consistently to womenssexual response. For many women, the

phases may vary in sequence, overlap, repeat, or be absent during some or all sexual encounters

SEXUAL DYSFUNCTION

Classification

• lack of desire (most common)

• lack of arousal

• anorgasmia

primary anorgasmia: never achieved orgasm under any circumstances

secondary anorgasmia:was able to achieve orgasms before but unable to achieve orgasms

presently

• dyspareunia: painful intercourse, can be superficial or deep

Etiology

• biological:

gynaecological (e.g.pregnancy, childbirth,menopausal atrophy, endometriosis, prolapse, urinary

incontinence)

urological (e.g. recurrent UTI,chronic renal failure)

vascular (e.g. peripheral vascular disease,CAD)

neurological dysfunction (e.g. nerve entrapment syndrome,spinal cord injury, multiple sclerosis,

Parkinsons)

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GY35 Gynaecology TorontoNotes 2023

• musculoskeletal (e.g. arthritis, mechanical back pain)

systemic health disorders(e.g. DM, thyroid disorders)

medication side effects(e.g. (3-blockers, benzodiazepines,SSRls, antipsychotics,oral

contraceptives)

• behavioural or lifestyle (e.g. smoking, alcohol consumption, opioids, obesity)

• psychological:

early events:history ofsexual violence, unpleasant early sexual experiences, or growing up in

a family orsociety that communicates no information or negative messages about women s

sexuality

current events: depression, anxiety, psychosis, fatigue,stress, or other mental health disorders

• relationship:

• abuse

• relationship distress

failure to engage in effective sexual stimulation

[ Dysparounia ]

£

^

MiJvni|m.il j

Dysparounia Cyclo

— Painful intercourse

(initially due to

organic etiology)

Introital

i

Endometriosis

Ailenomyosis

Leiomyomata/lihroids

PID (acute vs. chronic)

Hydrosalpinx

Tubo-ovarian abscess

Uterine retroversion

Ovarian cyst

Inadequate lubrication

Vaginismus

Rigid/intact hymen

Bartholin'

s or Skene'

s gland infection

Lichen sclerosis

Vulvovaginitis: atrophic ( hypoestrogen),

chemical, infectious (chlamydia, trichomoniasis)

Urethritis

Short vagina

Trigonitis

Congenital abnormality of the vagina

(e.g. vaginal septum)

Fear of pain

with intercourse 2°vaginismus

t

_.Anxiety with or J

withoutsexual

response

Figure 16. Approach to dyspareunia Figure 17. Dyspareunia cycle

Treatment

• general:

assess patient goals and construct a safety plan as needed

counseling

• lifestyle changes

• improve body image

• lack of desire:

• biological:rule out other conditions/medication side effects; consider sildenafil for SSRI side

effects;consider androgens(testosterone, DHEA), estrogens, tibolone in postmenopausal women;

consider serotonergic and dopaminergic agents:flibanserin, bupropion, buspirone; consider

bremelanotide

• psychological: rule out/treat depression, other mental health issues

relationship:assess couple interaction and partner sexual function; treat partner and relationship

conflict

• concerns with arousal/lubrication:

• biological:non-hormonal, water-based lubricants; consider estrogen (topical cream, tablet, or

ring)

psychological: address sexual anxieties

relationship:education regarding slowing of sexual response with aging

• anorgasmia:

biological:augmentstimulation ± vibrator; consider androgens

• psychological:sex education,

anxiety reduction, and use of erotica

• relationship:stimulation needs and helping patient leach partner what they need

• sexual pain disorders:

biological:rule out other conditions; topical estrogen if atrophy; consider nerve modulators

(amitriptyline, gabapentln, or pregabalin); pelvic floor physiotherapy

psychological:sex therapy if vaginismus

relationship:rule out abuse (with patient alone)

Kegel Exercises

Regular contraction and relaxation to

strengthen pelvic floor muscles

Reverse Kegel Exercises

1scontraction then 5s of relaxation

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*6 Gynaecology Toronto Notes 2023

Menopause

•see Family Medicine. FM43

Definitions

•lack of menses for 1 yr

•timing of menopause

• physiological; average age 51 yr (follicular atresia)

• premature ovarian insufficiency; before age 40 (autoimmune disorder, infection.Turner’s

syndrome)

iatrogenic (surgical/radiation/chemotherapy)

Menopause

Occurrence of last spontaneous

menstrual period,resulting from loss of

ovarian function (loss of oocyte response

to gonadotropins)

"Being in menopause "

Lack of menses for1yr

Clinical Features

•associated with estrogen deficiency

• vasomotor instability (tends to dissipate with time)

hot flushes/flashes, night sweats, sleep disturbances,formication, nausea, and palpitations

• urogenital atrophy involving vagina, urethra, and bladder (genitourinary syndrome of

menopause (GUSM))

dyspareunia, pruritus, vaginal dryness, bleeding, post-coital bleeding, urinary frequency,

urgency, and incontinence

inspection may reveal: thinning of tissues, erythema, petechiae, abrasions, and dryness on

speculum exam

Perimenopause

Period of time surrounding menopause

(2-8 yr preceding + 1yr after last

menses) characterized by fluctuating

hormone levels,irregular menstrual

cycles,and symptom onset

Menopause Pathophysiology

DegeneratingUieca cells fail to react to

endogenous gonadotropins (FSH,LH)

• skeletal

• osteoporosis, joint and muscle pain, and back pain

• skin and soft tissue

• decreased breast size, and skin thinning/loss of elasticity

• psychological

• increased anxiety, depression, irritability, fatigue, decreased libido, and memory loss

i

Less estrogen is produced

1

Decreased negative feedback on

liypolhalamic-pituitary-adrenal axis

Investigations 1

•for women with irregular cycles and menopausal symptoms:

>45 yr: no testing necessary

40-45 yr: p-hCG, prolactin,TSH

<40 yr: (5-hCG, FSH, prolactin, TSH

•increased levels of FSH (>35 IU/L) on day 3of cycle (ifstill cycling) and LH (FSH>LH)

•FSH level not always predictive due to monthly variation; use absence of menses for 1 yr to diagnose

•decreased levels of estradiol (later)

Increased FSH and LH

i

Stromal cells continue to produce

androgens as a result of increased

LH stimulation

Figure 18. Menopause

pathophysiology

Treatment

•goal is for individual symptom management

• 85%of women experience hot

flashes

• 20-30% seek medical attention

• 10% are unable to work

Table 17. Treatment of Menopause

Vaginal

Atrophy

Urogenital

Health

Osteoporosis Decreased

Libido

Vasomotor CVD'

Instability

Mood and

Memory

Menopause hormonal local estrogen: lifestyle

therapy (MHI) as first cream (Premarin '

changes(weight 1500 mg once

line. SSRI, venldlaxiiie, or Estragyn

gabapentin.

Calcium 1000- Vaginal lubricants, Manage CVD Anti depressants

counselling, risk factors (lirsl line). MHI

(augments

elfcct), CBT

loss, bladder daily,vitamin androgentraining), pelvic 0800 1000 ID. replacement

propanolol, donidine, Cream - ), vaginal floor exercises, weight- bearing testosterone

acupuncture. suppository local estrogen exercise,smoking cream or the oral

behavioural (VagiFems). replacement, cessation. form (Andriol 3)

modifications ring (Estring -). surgery

lubricants

Vaginal

bisphosphonales

(e.g.alendronate).

SERMs

(e.g.raloxifene

(E vista3)).HUT

(second-line

treatment)

(Replens:

).

intravaginal laser

'CVD (cardiovascular disease)

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GY37 Gynaecology Toronto Notes 2023

Menopause Hormone Therapy

• see family Medicine, IM I3

tong-Tcrm Hormone Therapy for Perlmcnopausal

and PostmenopausalWomen

Cocfcra-e DB Syst Per 2017:ttD004143

Purpose To determine tire effect of long-term HI

(hormone therapy) on mortality.cardiovascular

outcomes,cancer, gallbladder disease, fractures,

cognition,and quality ol life (001) inperimenopausal

and postmenopausal women.dunngHT use.andafter

cessatonofHT.

Results:22 studies with 43632 women included.

Host studies included postmenopausal American

women with at least some degree olcomorbidity,

with a mean participant age oner 60 yr.Combined

continuousHI:increased risk of coronary event

after1yr (from 2/1004 to 3-7/1000).venous

thromboembolism after 1yr (2/1000 to 4 11/1000).

stroke alter 3 yr (6/1000 to 6-12/1000).breast cancer

after 5.6 yr|19

'

1000 to 20-30/1000).gallbladder

disease after 5.6 yr (27/1000 to 38-60/10001,and

death from lungcancer after 5.6 yr use plus 2.4yr

additional follow up (5/1000 to 6-13/1000).Estrogen

onlyHI:increased risk ol venous thromboembolism

alter 1-2 yr use 12/1000 to 2-10/1000;alter 7 yr.

16/MOO to16-28/1000),stroke after 7 yr (24/1000

to 25-40/1000).and galtbi adder disease after 7 yr

use (27/1000 to 38-60/1400) but reduced the risk of

breast cancer alter 7yr (25 /1000 to 15 -25/1000 and

clinical fracture alter 7yr (141/1000 to 92-113/1000)

Women >65 yr olage taking combmed HI had shown

an increase in the incidenceof dementia after4

yr use(9/1000 to11-30/1004).for women with

cardiovascular disease,use of combined conbnuous

HIsigitifutilly increased the risk ol venous

thromboembolism al1yr (3/1000 to 3-29/1400).

Conclusions: HI may be contraindicated for some

women with increased risk of cardiovascular disease,

thromboembolic disease,and certain cancers socb

as breast cancer in women with a uterus.HIisnot

indicated lor pnmary or secondary prevention ol

cardiovascular disease,dementia,or deteriorationol

cognitive function.

Treatment Guidelines

• primary indication is treatment of menopausalsymptoms (vasomotor instability)

should not be prescribed if the only objective is the prevention of chronic disease

• before starting, review the benefits and risk (see Table 18) and contraindications with the patient

• use the lowest effective dose; patients with standard dose should be advised to lower dose after a few

years

• patients receiving MHT must be evaluated annually

• decisions around duration of treatment should be individualized, but recommended to avoid

treatment >5 yr with combination estrogen and progesterone treatment due to the durationdependent risk of breast cancer

• tapering and abruptly discontinuing MH'

l have similar impact on symptom recurrence, but

for patients with a history ofsevere baseline vasomotorsymptom, gradual tapering is probably

preferable

Table 18. MHT Benefits vs. Risks

Benefits Risks

Reduction of vasomotor symptoms

Reduction of sleep problems

Reduction of mood or anxiety problems

Reduction of aches and pains

Osteoporosis prevention and treatment

Reversal of vulvar and vaginal atrophy (local eslrogen therapy

recommended ilsuch atrophy is the only Indication for therapy)

Ihromboemholic events

Stroke

Breast cancer (increased risk after 4-5 yr with estrogen-progesterone

regimens,noincreased risk (oral least 8 yr with estrogen-alone

regimens)

Coronary heart disease (for women age >60 and those who are >10 yr

after menopause)

Endometrial hyperplasia and cancer (with estrogen-only regimens)

MHT Components

• estrogen

• oral or transdernial (e.g. patch, gel)

• transdernial preferred for women overall, especially with hypertriglyceridemia or impaired

hepatic function,smokers, and women who suffer from headaches associated with oral MHT, due

to decrease risk of VTE

low-dose (preferred dose: Premarin'0.3 mg/Estradot* patch 25 pg, can increase if necessary)

• progestin

given in combination with estrogen for women with an intact uterus to prevent development of

endometrial hyperplasia/cancer

(and

Moderatc

inadequate

- toresponse

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to bchavioural

flashes end

/lifcstyle

/or night

modifications

sweats

)

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