Female Sexual Dysfunction + infertility Flashcards
1
Q
general causes of female sexual dysfunction (4)
A
- medical disease
- pharmacological treatment
- medical therapy/surgical procedures
- past/ongoing psychological factors
2
Q
Pharmacological treatment - SSRIs on F sexual dysfunction
A
increase 5-HT in brain, may alter PNS outflow.
-may suppress DA, which is needed for arousal/libido
3
Q
how pelvic radiation (med therapy) may affect sexual dysfunction?
A
tissue damage => sexual pain
- inappropriate lubrication
4
Q
how hysterectomies may effect sexual dysfxn
A
uterus removed.
- may damage nerves = sexual pain
- may have psychological impact
5
Q
cancer treatment on sexual dysfunction
A
- survival > repro
- atrophy of vagina, accummulation of fibrotic tissue = stiffened, or brittle.
- psychological impact
6
Q
what is desire disorder?
A
inability to recognize sexual desire - no/ lack of arousal to variety of stimuli
- disconnect between cognitive and physiological phenomena
7
Q
desire disorder study
A
- vaginal pulse amplitude: shows whether there’s increase in blood flow that’s assoc w arousal
- subject engages in fantasy, or listens to tape/film
- normal control will increase arousal when engaging in fantasy
- in desire disorder, physical stimulus triggers arousal, fantasy did not increase arousal
8
Q
implications of desire disorder study
A
- cog inputs are important for W. genital feedback is more important later on.
9
Q
what is sexual pain in females?
A
persistent, recurring pain with attempted or complete vaginal entry
- no lubrication, inflammation/infection, damage to tissue, uterine prolapse (slipped down, displacing ligaments that hold it in place), sexual fears/inhibitions
10
Q
what is vaginismus?
A
persistent/recurrent difficulty to allow vaginal penetration despite desire to do so.
- painful spasms/involuntary contraction of outer 1/3 of vaginal wall + surrounding muscles
11
Q
causes of vaginismus?
A
psychological: fear of coitus, frustration with partner
- organic cause: scar tissue build-up
12
Q
what is cycle of pain
A
- anticipate pain
- dont relax muscle
- lack of relaxation = pain
- pain increases muscle contraction
- body braces for pain
- avoid sex + lower libido
13
Q
therapy for vaginismus?
A
- biofeedback: pain elimination technique
- kegel excercises: control pelvic floor muscles
- desensitization with insertion + dilation training
14
Q
what is orgasmic dysfunction?
A
inability to orgasm.
- only problem if it feels like a problem. can be sexually gratified anyway
- primary: never had orgasm (10%)
- secondary: fail to reach in selective situations (20%)
- partly genetic basis
15
Q
cause of orgasmic dysfunction?
A
psych input: central descending input inhibits orgasm
physio basis is rare - low blood flow to repro, illness, fatigue, aging/menopause, absence of E (low libido, less maintenance of repro tissue can = sexual pain), diabetes (loose small vessels that supply repro tissue = less pleasure)
16
Q
treatments for organic dysfxn
A
- E treatment has too many side effects. may do Androgen treatment (limited success)
- viagra: increase blood flow, once there is arousal
- clitoral suction device: increase blood flow + sensation
17
Q
4 types of female genital mutilation
A
1: clitoridectomy: removal of clitoral hood
2: excision: removal of clit entirely
3: infibulation: removal of clitoral hood, labia majora, minora and sometimes complete closure of vulva - leaving a small opening.
4. all other modification that is non-medical and potentially harmful (symbolic cutting to signify womanhood)
18
Q
the more imminent physiological and psychological impacts of female genital mutiliation
A
- trauma
- bleeding (hemorrhage at ime of, or when healing., circulatory shock/death = consequences
- infection, sepsis => chronic pelvic infection can lead to infertility
- urine retention: difficult, impossible to urinate; obstructed urethra, pain/fear of urination
- damage to urethra, vagina, perineum, rectum =may lead to incontinence
19
Q
subsequent physiological impact of female genital mutiliation
A
- difficult/impossible intercourse or gyno
- difficult to birth baby, need de-infubulation
- keloid, cyst formation
- menstrual complications
- recurrent urinary tract infection
- chronic pelvic inflammatory disease
- complications with pregnancy
- prolonged labour
- repeated de-infibulation/re-infibulation
20
Q
what is a keloid/cyst (fgm)
A
scar tissue or cyst that forms may grow in the uterus. causeing difficult intercourse, birth complications.
- suspicion of infertility
21
Q
why may there be menstrual complications assoc with fgm?
A
occlusion of vaginal opening may not permit blood to exit.
- painful
accumulation or blood may cause inflammation + distention of the abdomen
22
Q
why may miscarriage be fatal?
A
products of conception cannot leave the body after miscarriage. may lead to infection, can be fatal
23
Q
define female infertility
A
inability to become pregnant following 1 year without the use of contraception
24
Q
risk factors in infertility?
A
aging, anovulation, endometriosis, PCOS, tubal block, implantation failure, impaired sperm, sperm antibodies, stress/excercise, eating disorders, seasonality?
25
aging impacts on fertility
most fertile at 20 years.
- infertility increases with age, sharp increase in infertility at age 35.
- may need clinical intervention
26
define amenorrhea
absence of menstruation for 3+ months
| - failure to menstruate by age 16
27
define oligomenorrhea
infrequent/irregular menses.
| - may indicate anovulation
28
amennorrhea in intact genital outflow tract
- indicates HPG axis failure
29
what is anovulation
irregular or absent menstrual periods due to lack of ovulation
30
possible causes of anovulation
- severe stress
- excessive exercise
- extremes of body fat content
- substance misuse disorders
31
malfunction at hypothalamic/pituitary level causing anovulation
low secretion of GnRH, low pulse rate, low amplitude, low Gn. if not enough LH - no LH surge = no ovulation.
32
treatment for anovulation @hypothalamic level
pulsatile GnRH stimulatory agonists
33
Anovulation due to pit function
- no adequate production of FSH +LH, despite normal levels of GnRH
34
treatment for anovulation due to pit function
Clomid
- weak Estrogen effect.
- higher dose = anti-E effect. (suppress E negative feedback to decrease suppression of Gn release)
- if high FSH/LH: may stimulate more than 1 ovum to maturation + ovulation. increased chance of hyperstimulation + multiple babies.
- other side effects: hot flashes, mood swings, headaches, visual disturbances, ovarian cysts.
35
anovulation due to pit insufficiency - if clomid ddoesnt work?
PERGONAL:
Gn administration
+ hMG and hCG
-- injection of combo therapy. highly effective
- hMG: high FSH + LH, produces in women with menopause. produces less endogenous E, less (-) feedback.
- hCG injected at specific time to act as LH, boosts to trigger ovulation
36
side effects of pergonal
- ovarian hyperstimulation syndrome
- - enlarged ovaries
- - increased pressure in abdomen, pain, discomfort, bloating, shortness of breath.
- - immediate medical intervention
37
anovulation + prolactin
- excessive Pl secretion. DA suppresses Pl + protects from hyperprolactanemia.
- if take SSRI, may suppress DA = no suppression of PI = excessive production of Pl.
- Pl acts to suppress GnRH and downstream = (-) ovarian function
38
treatment for hyperprolactanemia
prolactin inhibitor
- restores fertility
- DA inhibitors can cause hyperprolactinemia, infertility.
39
anovulation due to ovary not responding to LH/FSH?
| - causes?
- endometriosis
- ovarian cysts (fluid filled, accumulation of fibrotic tissue, impair ovulation
- tumors
- scars caused by ovarian infection
-- require surgical intervention
40
define endometriosis
endometrial tissue outside the uterine cavity
| - retrograde menstruation
41
when does endometriosis become an issue?
when the tissue moves in retrograde, the body recognizes it as a wound and heals it with angiogenesis (increased blood flow)
- lesions resemble endometrial tissue in uterus (same cycle)
42
symptoms of endometriosis
inflammation, severe pain, dysmenorrhea, chronic pelvic pain, sexual pain, infertility
43
discuss the neuro-endo-immune interactions assoc with endometriosis
all 3 communicate with each other.
1. macrophage releases pro-inflammatory cytokines into circulation.
2. PIC increase E production at enometrial cells
3. E increases proliferation + changes to secretory phenotype to increase P
4. increase in E can act on macrophage to exacerbate PIC production.
5. receptor for PIC assoc with sensory nerves. (PIC binding = pain on nerves)
6. vicious cycle of E -> PIC and pIC -> E
7. macrophage hits neurotrophic effects too to increase nerve growth factors + increase nerve endings = heightened pain response
44
what is most common form of endometriosis? consequence?
ovarian
- if accummulate on ovary, no ovulation because ovum cant get to surface.
- difficult to deal with clinically. surgical diagnosis + intervention.
45
treatment of endometriosis?
- symptom management
- - medication: oral contraceptives; hypoestrogenic state (GnRH antagonist, aromatase inhibitor = reduce E at higher levels)
- surgical therapy: for intractable pelvic pain
- - excision/removal of ectopic endometrial tissue
- - uterosacral nerve ablation (if nerve is destroyed/re-innervation becomes painful)
- hysterectomy/ooporectomy
46
some potential causes of anovulation
- permanent ovarian malfunction
- Turner's Syndrome (XO - no follicles in ovaries)
- Polycistic Ovary syndrome
47
what is PCOS?
many immature follicles, fibrosis, fluid filled follicles with no ovum
48
most accepted theory for PCOS
1. increase A predisposes to abdominal adiposity
2. abdominal adiposity predisposes to insulin resistance
3. high insulin resistance increases circulating glucose levels
4. high circulating glucose = hyperglycemia
5. hyperglycemia = increase insulin release from pancreas
6. hyperinsulanemia
7. insulin act on pituitary to increase LH production
7a. insulin acts on theca cells to increase A and restart cycle
7b. LH act on theca cells to increase A too.
8. insulin acts on liver. suppresses steroid-hormone-binding-globulin (more circulating A)
49
characteristics of PCOS
high circulating A
high circulating LH
hyperinsulanemia
hyperglycemia
50
effects of excess androgen secretion
- reduced E
- high LH (adiposity, insulin)
- low FSH so LH:FSH is off
- insulin resistance (exacerbates obesity)
51
other effects of PCOS
menstrual disorders, increased prevalence of obesity + insulin resistance
- anovulation
- infertility
52
in overweight PCOS patients, how does weight loss help?
may restore fertility
- energy expenditure, + burning fat.
- adipose cells produce leptin = leptinemia when overweight.
- too much or too little leptin interferes with GnRH secretion.
- may normalize Gn levels, restore menstrual cycle
53
granulosa cell aromatase in PCOS
high A and low E
- normally, granulosa converts A -> E.
- in PCOS, aromatase may have malfunction..
- low FSH so, not much proliferation of granulosa = less aromatase, less conversion = more A
54
inhibin in PCOS
(-) feedback on ant.pit. to suppress FSH levels
| - FSH decreases
55
treatment for PCOS
- drugs that sensitize to insulin (less resistance) = metformin
- E/P = normalize LH and increase SerumHBG
56
what is tubal blockage
blockage of one or both oviducts
- ovulation occurs but sperm cannot reach the ovum
- fertilized ovum cannot reach uterus.
2nd leading cause of infertility
57
potential causes of tubal blockage
kink
- scarring (STI, causing pelvic inflammatory disease)
- endometriosis on tubes
58
treatment for tubal blockage
- surgery
- - introduce fluid or gas into oviducts.
- laparotomy/laparoscopy: inject saline/gas to expand the abdomen
- -removal of adhesions
- - transcervical balloon tuboplasty
- bypass oviducts + do IVF
59
what is absence of implantation?
pre-embryo may reach uterus but implantation does not occur
60
what's needed for implantation?
uterus must be primed with E+P for implantation
61
what is treatment for absence of implantation
priming may be inadequate
| - treat with E+P
62
damaged endometrium + absence of implantation
- fibroids, scars
- improperly performed abortion (scraped base layer off)`
- inflammation/infection
63
what are uterine fibroids
collection of fibrous tissue located in many areas.
- may distort architecture of uterus. may disrupt proliferation + development of endometrium as result, making implantation difficult/impossible.
- can be removed if causing issues
64
causes of reduced sperm transport in females
- acidity of vaginal enviro
- cervical mucus is hostile
- damaged cervix
65
treatment for reduced sperm transport in females
alkaline douche - assist sperm in viability
E administration: thins cervical mucus to watery consistency. forms channel in cervix to facilitate fertilization
surgery for damaged cervix (usually after infection)
66
females + sperm antibodies
if not exposed to sperm/semen before, upon exposure may develop antibodies that target sperm and become allergic. to sperm.
-best option: donor sperm
67
stress/exercise + fertility
chronic stress /exercise disupts repro fxn
- impair HPG axis function + libido
68
HPa and HPG axis interact in stress/exercise and fertility
- hypothal releases CRH
- pit released ACTH
- adrenal gland releases cortisol
- Hypothal releases O, Pl, V - all inhibitory on hypothal and Gn
treat: CRH antagonist
69
endorphins + fertility
released upon excercise/stress
= suppress GnRH release.
treat with naloxone = restore HPG
70
2 eating disorders
anorexia nervosa: psychosomatic disorder (extreme weight loss, body image disturbance, fear of weight gain)
bulemia: over-consumption, restriction, binging, purging
71
neuroendocrine perspective on eating disorders *common thread btw the two*
- Gn sectretion matches pre-pubertal pattern (low LH + FSH)
- hyperactivation of HPA (because intense stressor = cortisol inhibits HPG)
- lasting anovulation after re-gaining weight. may be irreversible
- increased central opioid activity (link to eating, LH release with naloxone,
72
thyroid disorders + menstrual abormalities
- early 1900's.
- hemorrhage, amenorrhea, oligomenorrhea, repro failure (carrying to term or lactation)
- repro symptoms may appear before other thyroid symptoms
73
HP-thyroid and HPG axes are dependent
thyroptropin (TRH) in median eminence + PVN of hypothalamus. release hormones close to GnRH-releasing neurons.
TRH receptors found on human oocytes + granulosa cells
74
TRH and Pl
TRH stimulates near lactorophic neurons. may stimulate them by accident = PL release (in excess)
75
DA and HPT, HPG
decreased DA
| = less suppression on PL, increased PL, decrease TSH and LH
76
what is hypothyroidism + what are the effects?
too little thyroid.
- interferes with pulsatile GnRH release (Thyroid may act on GnRH/kisspeptin neuron)
-reduced Estrogen metabolism (more E - more (-) feedback), increased A - more (-) feedback
77
what is seasonality of fertility?
seasonal pattern of human conception + birth rate.
- more conception in colder months, more births in warmer months
78
what reduces seasonality of fertility?
| - what does this allow for?
domestication, resource security.
- provides constancy, not seasonality
- allows for continuous sexual activity. altho some patterns remain
79
implications of seasonality on infertility?
may be better chances of conception in certain months (colder)
- maybe thru assisted repro, best if done during those cold months
80
how seasonality may impact fertility?
- hypothalmo-pituitary output may increase
- pineal gland: melatonin decreased, improves repro function.
- adrenal output: decrease in winter?
- 5-HT decrease in winter?
81
seasonality + ovum/sperm quality
- quality, timing of ovulation = higher quality, more optimal timing
- greater receptivity of endometrium
- quality and quantity of sperm: more concentration, move faster in W than in Summer
- reduction of coitus
