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PHYSL 400 - Repro > Female Sexual Dysfunction + infertility > Flashcards

Female Sexual Dysfunction + infertility Flashcards

1
Q

general causes of female sexual dysfunction (4)

A
  1. medical disease
  2. pharmacological treatment
  3. medical therapy/surgical procedures
  4. past/ongoing psychological factors
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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

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3
Q

how pelvic radiation (med therapy) may affect sexual dysfunction?

A

tissue damage => sexual pain

  • inappropriate lubrication
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4
Q

how hysterectomies may effect sexual dysfxn

A

uterus removed.

  • may damage nerves = sexual pain
  • may have psychological impact
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5
Q

cancer treatment on sexual dysfunction

A
  • survival > repro
  • atrophy of vagina, accummulation of fibrotic tissue = stiffened, or brittle.
  • psychological impact
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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
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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
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8
Q

implications of desire disorder study

A
  • cog inputs are important for W. genital feedback is more important later on.
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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

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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
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11
Q

causes of vaginismus?

A

psychological: fear of coitus, frustration with partner

- organic cause: scar tissue build-up

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12
Q

what is cycle of pain

A
  1. anticipate pain
  2. dont relax muscle
  3. lack of relaxation = pain
  4. pain increases muscle contraction
  5. body braces for pain
  6. avoid sex + lower libido
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13
Q

therapy for vaginismus?

A
  • biofeedback: pain elimination technique
  • kegel excercises: control pelvic floor muscles
  • desensitization with insertion + dilation training
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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
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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)

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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
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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)

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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
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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
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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
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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

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22
Q

why may miscarriage be fatal?

A

products of conception cannot leave the body after miscarriage. may lead to infection, can be fatal

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23
Q

define female infertility

A

inability to become pregnant following 1 year without the use of contraception

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24
Q

risk factors in infertility?

A

aging, anovulation, endometriosis, PCOS, tubal block, implantation failure, impaired sperm, sperm antibodies, stress/excercise, eating disorders, seasonality?

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25
Q

aging impacts on fertility

A

most fertile at 20 years.

  • infertility increases with age, sharp increase in infertility at age 35.
  • may need clinical intervention
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26
Q

define amenorrhea

A

absence of menstruation for 3+ months

- failure to menstruate by age 16

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27
Q

define oligomenorrhea

A

infrequent/irregular menses.

- may indicate anovulation

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28
Q

amennorrhea in intact genital outflow tract

A
  • indicates HPG axis failure
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29
Q

what is anovulation

A

irregular or absent menstrual periods due to lack of ovulation

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30
Q

possible causes of anovulation

A
  • severe stress
  • excessive exercise
  • extremes of body fat content
  • substance misuse disorders
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31
Q

malfunction at hypothalamic/pituitary level causing anovulation

A

low secretion of GnRH, low pulse rate, low amplitude, low Gn. if not enough LH - no LH surge = no ovulation.

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32
Q

treatment for anovulation @hypothalamic level

A

pulsatile GnRH stimulatory agonists

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33
Q

Anovulation due to pit function

A
  • no adequate production of FSH +LH, despite normal levels of GnRH
34
Q

treatment for anovulation due to pit function

A

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
Q

anovulation due to pit insufficiency - if clomid ddoesnt work?

A

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
Q

side effects of pergonal

A
  • ovarian hyperstimulation syndrome
    • enlarged ovaries
    • increased pressure in abdomen, pain, discomfort, bloating, shortness of breath.
    • immediate medical intervention
37
Q

anovulation + prolactin

A
  • 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
Q

treatment for hyperprolactanemia

A

prolactin inhibitor

  • restores fertility
  • DA inhibitors can cause hyperprolactinemia, infertility.
39
Q

anovulation due to ovary not responding to LH/FSH?

- causes?

A
  • endometriosis
  • ovarian cysts (fluid filled, accumulation of fibrotic tissue, impair ovulation
  • tumors
  • scars caused by ovarian infection

– require surgical intervention

40
Q

define endometriosis

A

endometrial tissue outside the uterine cavity

- retrograde menstruation

41
Q

when does endometriosis become an issue?

A

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
Q

symptoms of endometriosis

A

inflammation, severe pain, dysmenorrhea, chronic pelvic pain, sexual pain, infertility

43
Q

discuss the neuro-endo-immune interactions assoc with endometriosis

A

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
Q

what is most common form of endometriosis? consequence?

A

ovarian

  • if accummulate on ovary, no ovulation because ovum cant get to surface.
  • difficult to deal with clinically. surgical diagnosis + intervention.
45
Q

treatment of endometriosis?

A
  • 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
Q

some potential causes of anovulation

A
  • permanent ovarian malfunction
  • Turner’s Syndrome (XO - no follicles in ovaries)
  • Polycistic Ovary syndrome
47
Q

what is PCOS?

A

many immature follicles, fibrosis, fluid filled follicles with no ovum

48
Q

most accepted theory for PCOS

A
  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
Q

characteristics of PCOS

A

high circulating A
high circulating LH
hyperinsulanemia
hyperglycemia

50
Q

effects of excess androgen secretion

A
  • reduced E
  • high LH (adiposity, insulin)
  • low FSH so LH:FSH is off
  • insulin resistance (exacerbates obesity)
51
Q

other effects of PCOS

A

menstrual disorders, increased prevalence of obesity + insulin resistance

  • anovulation
  • infertility
52
Q

in overweight PCOS patients, how does weight loss help?

A

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
Q

granulosa cell aromatase in PCOS

A

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
Q

inhibin in PCOS

A

(-) feedback on ant.pit. to suppress FSH levels

- FSH decreases

55
Q

treatment for PCOS

A
  • drugs that sensitize to insulin (less resistance) = metformin
  • E/P = normalize LH and increase SerumHBG
56
Q

what is tubal blockage

A

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
Q

potential causes of tubal blockage

A

kink

  • scarring (STI, causing pelvic inflammatory disease)
  • endometriosis on tubes
58
Q

treatment for tubal blockage

A
  • 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
Q

what is absence of implantation?

A

pre-embryo may reach uterus but implantation does not occur

60
Q

what’s needed for implantation?

A

uterus must be primed with E+P for implantation

61
Q

what is treatment for absence of implantation

A

priming may be inadequate

- treat with E+P

62
Q

damaged endometrium + absence of implantation

A
  • fibroids, scars
  • improperly performed abortion (scraped base layer off)`
  • inflammation/infection
63
Q

what are uterine fibroids

A

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
Q

causes of reduced sperm transport in females

A
  • acidity of vaginal enviro
  • cervical mucus is hostile
  • damaged cervix
65
Q

treatment for reduced sperm transport in females

A

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
Q

females + sperm antibodies

A

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
Q

stress/exercise + fertility

A

chronic stress /exercise disupts repro fxn

  • impair HPG axis function + libido
68
Q

HPa and HPG axis interact in stress/exercise and fertility

A
  • 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
Q

endorphins + fertility

A

released upon excercise/stress
= suppress GnRH release.

treat with naloxone = restore HPG

70
Q

2 eating disorders

A

anorexia nervosa: psychosomatic disorder (extreme weight loss, body image disturbance, fear of weight gain)

bulemia: over-consumption, restriction, binging, purging

71
Q

neuroendocrine perspective on eating disorders common thread btw the two

A
  • 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
Q

thyroid disorders + menstrual abormalities

A
  • early 1900’s.
  • hemorrhage, amenorrhea, oligomenorrhea, repro failure (carrying to term or lactation)
  • repro symptoms may appear before other thyroid symptoms
73
Q

HP-thyroid and HPG axes are dependent

A

thyroptropin (TRH) in median eminence + PVN of hypothalamus. release hormones close to GnRH-releasing neurons.

TRH receptors found on human oocytes + granulosa cells

74
Q

TRH and Pl

A

TRH stimulates near lactorophic neurons. may stimulate them by accident = PL release (in excess)

75
Q

DA and HPT, HPG

A

decreased DA

= less suppression on PL, increased PL, decrease TSH and LH

76
Q

what is hypothyroidism + what are the effects?

A

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
Q

what is seasonality of fertility?

A

seasonal pattern of human conception + birth rate.

  • more conception in colder months, more births in warmer months
78
Q

what reduces seasonality of fertility?

- what does this allow for?

A

domestication, resource security.
- provides constancy, not seasonality

  • allows for continuous sexual activity. altho some patterns remain
79
Q

implications of seasonality on infertility?

A

may be better chances of conception in certain months (colder)
- maybe thru assisted repro, best if done during those cold months

80
Q

how seasonality may impact fertility?

A
  • hypothalmo-pituitary output may increase
  • pineal gland: melatonin decreased, improves repro function.
  • adrenal output: decrease in winter?
  • 5-HT decrease in winter?
81
Q

seasonality + ovum/sperm quality

A
  • 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

PHYSL 400 - Repro (20 decks)

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