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week 23: irregular menstruation > general IM > Flashcards

general IM Flashcards

1
Q

list menopausal symptoms

A
  • hot flushes
  • night sweats
  • insomnia
  • joint aches
  • dyspareunia (painful sex )
  • loss of libido
  • vaginal dryness
  • anxiety
  • poor concentration
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2
Q

red flags in gynae Hx and possible sinister cause

A
  • ascites, bloating, abdo pain, irregular bleeding, w.loss =think ovarian cancer (blood test = cal25, disease marker, not diagnostic)
  • PMB in >55 think endometrial cancer!
  • PCB, IMB, mass in cervix think cervical cancer
  • pelvic pain, vagina discharge, fever, irregular bleeding = think PID
  • acute severe lower abdo pain, hypovolemic shock = think cystic torsion
  • abnormal persistent growing skin lesion (ulcer, lump) = vulval cancer
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3
Q

what advice would you give a menapausal pt who is anxious about starting HRT because of concerns about the therapy and some high profile new stories

A

benefits:

  • symptom control
  • quality of life
  • reduced osteoporotic fracture
  • reduced bowel cancer
  • possibly protective Alzeimer’s and parkinsons
  • HRT <10years after menopause = fewer risks and less CV events

risks:

  • VTE
  • stroke risk
  • increased risk of breast cancer (contraindicated in pt’s with Hx of breast/womb/ ovarian cancer)
  • increased risk of endometrial cancer if unopposed oestrogen
  • gallbladder disease
  • HRT >20 years after menopause greater risk of harm

> can stop at any point!!
high risk of CVD or diabetes - conrol risk factors and non-hormonal Rx first
high risk of DVT (obesity/diabetes) - transdermal patches

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4
Q

what are the 2 treatment regimens for HRT therapy?

A
  • comprises oestrogen and progesterone (oestrogen alone only okay in pt without uterus)

1) CONTINUOUS regimens - low dose oestrogen (estridiol, estriol) and progestin are taken daily. amenorrhea; therefore recommended in pts with amenorrhoea for >12mnths
2) SEQUENTIAL - progestin is added to oestrogen cyclically for 10-14 days each month. used in perimenopausal women. still get a bleed

*taken for 5years and looked at weaning off. Depends on pt and their ICE!!

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5
Q

what is the hormone that leads to an increase in FSH and LH secretion at puberty (males and females)?

A

GnRH- gonadotrophin releasing hormone

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6
Q

describe the events of male puberty

A
  • bursts of GnRH release begins in age 8-12 to initiate puberty
  • FSH and LH release triggers testes to produce androgens (sex hormones) and sperm
  • frequency of burst continue until levels of GnRH, FSH, LH and testosterone are same as adult
  • testosterone produces secondary sexual features (testicular enlargement, pubic hair growth, deepening of voice, growth of larynx)
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7
Q

describe the events of female puberty

A
  • adrenarche (discussed on another card) then menarche (next card)
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8
Q

what is meant by ‘menarche’ and explain likely triggers and timescale for onset

A
  • the first occurrence of menstruation and therefore start of the ability to produce mature ova and an endometrium that could support a zygote
  • onset usually 10-16 years old
  • onset related to critical level of body fat –> triggers GnRH
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9
Q

what triggers somatic growth in both males and females (2years earlier)

A

gonadal sex hormones, growth hormones and insulin-like growth factor

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10
Q

adrenarche is the earliest stage in sexual maturation (6-8years) in both males and females. what hormones trigger this and what changes are observed?

A
  • androgens from the adrenal gland (e.g. dehydroepiandrosterone)
  • cause growth spurt
  • start of pubic hair growth
  • breast development in females
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11
Q

what is the difference between an ovarian cycle and menstrual cycle?

A

ovarian:

  • production and release of ova
  • lasts 28days
  • has 2 phases: follicular (day 1-14) associated with maturation of the egg and luteal associated with ovulation and development of corpus luteum

menstrual:
- signified by blood loss through vagina due to sloughing of uterine endometrial lining if not required for pregnancy

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12
Q

what are the hormonal changes during the female sexual cycle each month?

A
  • GnRH pulses trigger the release of FSH and LH from anterior pituitary
  • affects follicular development
  • the maturating follicle secretes oestrogen -> inhibits FSH
  • high levels of oestrogen causes a spike in LH which triggers ovulation
  • as ovulation occurs oestrogen levels fall due to degeneration of the follicle
  • the developing corpus luteum secretes oestrogen (at lower levels than before) and progesterone (higher conc than oestrogen)
  • progesterone inhibits FSH and LH and produces environment for implantation (endometrium)
  • corpus luteum degenerates if no pregnancy causing low levels of oestrogen and prog –> sloughing of uterine lining and allows increase in FSH and LH
  • cycle starts again
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13
Q

define menopause

A

begins 12months! after the end of the last menstrual bleed

  • cessation of menstruation - commonly occurs between 45 and 55 years
  • not a disease
  • due to low levels of oestrogen
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14
Q

what are the potential triggers of menopause?

A
  • oocyte depletion
  • remaining follicles not sensitive to LH/FSH
  • age related changes in CNS that alter GnRH
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15
Q

what are the physiological changes during menopause?

A
  • perimenopause: irregular menstrual cycle
  • progressive changes = ovary atrophy (few or no healthy follicles), decrease in oestrogen (concomitant increase in FSH and LH), breast and reproductive tract atrophy, vaginal dryness, hot flushes, increase bone mineral loss, increase CV risk
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16
Q

what is the dominant oestrogen pre and post menopause?

A 
pre = beta-oestradiol (most potent and principal oestrogen secreted by the ovary)
post = estrone
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17
Q

what are the 4 stages of sexual arousal?

A

1)excitement, 2)plateau, 3)orgasm, 4)resolution

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18
Q

semen secreted into the prostatic urethra is known as?

A

emission

*expulsion = ejaculation into vagina

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19
Q

which male accessory organ supplies fructose to semen?

A

seminal vesicle

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20
Q

describe the in vivo fertilisation of gametes

A

pre-fertilisation:

  • oocyte viable 6-24hrs after ovulation
  • spermatozoa viable 24-48hrs in reproductive tract
  • spermatozoa incapable of fertilisation until they undergo CAPACITATION (removal of glycoprotein coat) in reproductive tract
  • allurin secreted by mature ovum to attract sperm
  • sperm attaches to egg by protein called fertillin via integrin
  • acrosomal reaction occurs so sperm can penetrate egg
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21
Q

fusion of the sperm and egg triggers 3 events. what are they?

A

block to polyspermy:

  1. primary block - egg membrane depolarises, preventing other sperm fusing
  2. secondary block - changes to zona pelucida making sperm binding difficult (cortical reaction)
  3. 2nd meiotic division of egg
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22
Q

describe the process of implantation

A

sticky blastocyst attaches to endometrium –> trophoblast releases proteases –> trophoblast cells grow into endometrium via pathways created –> trophoblast releases nutrients for embryo –> boundaries between trophoblast cells disintegrate “syncytiotrophoblast” will become foetal placenta –> trophoblast induces ‘decidualization’ of endometrium - increased local vascularisation and nutrient storage –> blastocyst becomes buried in uterine lining by day 12

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23
Q

basic endocrinology of the maintenance of pregnancy

A

1st trimester:

  • human chorionic gonadotropin -> produced by blastocyst, prolongs the corpus luteum which continues to grow and increases concentration of progesterone and oestrogen (maintain uterine lining)
  • after 10 weeks the placenta produces these hormones

2nd/3rd trimester:

  • oestrogen and progesterone take over
  • oestrogen stimulates growth of myometrium musculature (expel foetus during labour) and development of mammary gland ducts
  • progesterone suppresses contractions of uterine myometrium

other endocrine factors:

  • human chorionic somatomammotropin (hCS) -> prepares breast glands for lactation
  • parathyroid hormone-related peptide -> mobalises maternal Ca2+ for calcification of foetal bones
  • relaxin -> softens cervix, loosens pelvic connective tissue
  • placental corticotropin releasing hormone (CRH) -> stimulates DHEA production by foetal adrenal cortex - important in initiation of parturition
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24
Q

what is the MoA of oestrogens?

A

MoA = interact with nuclear receptors to generate gene transcription (some interact with membrane receptors - raid vascular actions). effects depend on sexual maturity! e.g. in primary hypogonadism stimulates development of secondary sexual characteristics and in menopause prevents against symptoms

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25
Q

what are the therapeutic uses of oestrogen?

A

1) replacement therapy - promote sexual maturation in POI (Turners syndrome) or menopausal symptoms such as flushing, vaginal dryness and osteoporosis
2) as contraception - single or in combo with progesterone
3) prostate and breast cancer (usually androgen dominant)

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26
Q

give an example of a natural and synthetic type of oestrogen?

A 
natural = estridiol, estriol 
synthetic = mestranol, ethinylestradiol
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27
Q

what are some of the side effects of therapeutic oestrogen?

A

breast tenderness, nausea, vomiting, anorexia, retention of salt and water with resultant oedema and increased risk of thromboticembolism (increased coagulability)

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28
Q

give examples of selective oestrogen receptor modulators (drugs that are selective oestrogen agonists in some tissues but antagonists/ANTI-OESTROGENS in others)

A
  1. Tamoxifen - ant. in mammary tissue, ag. in bone
  2. Raloxifene - ant. in breast and uterus, ag. in bone
  3. Clomiphene - ant. at hypothalamus and pituitary (increased gonadotrophin secretion, increased oestrogen and ovulation: e.g. used in Rx of infertility in PCOS)
29
Q

what is the MoA of progesterones?

A

act on progesterone receptors to regulate gene transcription in target tissues (+ inhibit synthesis of oestrogen receptors)

30
Q

natural progesterone is not used therapeutically as it has a rapid clearance. give example of synthetic derivatives (PROGESTINS) which can be used instead

A

medroxyprogesterone + hydroxyprogesterone

  • testosterone derivatives = norethisterone or ethynodiol
  • newer progestogens that have less androgenic activity = desogestrel and gastodene
31
Q

what are the therapeutic uses of progestogens

A

1) OCP - alone or in combo with oestrogen
2) other forms of contraception - progesterone only injectible or implantable or part of interuterine
3) combined with oestrogen in HRT (in women with intact uterus) to prevent endometrial hyperplasia, carcinoma, endometriosis

32
Q

what are some side effects of progestogens?

A

acne, fluid retention, weight gain, depression, change in libido, breast discomfort, menstrual cycle irregularity and increased thromboembolism risk

33
Q

what ANTI-PROGESTERONE drug can be used in combo with prostaglandin analogues as an effective medical alternative to surgical termination of early pregnancy?

A

mifepristone

34
Q

what is the MoA of the combined oral contraceptive pill (e.g. ethinyloestadiol + norethisterone)?

A
  • oestrogen inhibits FSH supressing development of ovarian follicle
  • progestin inhibits LH stopping ovulation!
  • together alter endometrium to discourage implantation
  • main action is to stop ovulation
  • taken for 21 days with 7 free days: withdrawal-bleed
35
Q

what is the action of the progesterone only pill (e.g. norethisterone, levonorgestrel or ethynodiol diacetate)

A
  • primarily works by thickening the cervical mucus (inhospitable to sperm)
  • also has affects on the endometrium and fallopian tube motility –> hinders implantation

*taken daily without interruption

36
Q

what are the side effects of the COCP?

A
  • nausea, flushing, dizziness and bloating
  • weight gain, skin changes, depression or irritability
  • small number of women develop reversible hypertension
  • small increase in risk of thromboembolism
37
Q

why would you use the mini pill over COCP?

A

if oestrogen containing pills are contraindicated or if pt’s blood pressure rises unacceptably during Rx during use of COCP

38
Q

what other methods of contraception could you offer?

A

long acting progesterone only contraception:
- medroxyprogesterone–> IM injection every 3 months- levonorgestrel–> subcutaneous implant or impregnates IUD

post-coital emergency contraception:

  • oral administration of levonorgestrel (progestin) alone or in combo with oestrogen
  • effective if taken within 72hrs and repeated 12 hours later
39
Q

what is the reproductive effect of androgens + what is its therapeutic use?

A

reproductive:

  • testosterone is the main androgen (produced by Leydig cells in testes and in small amounts in the adrenal cortex and ovaries)
  • LH stimulates androgen secretion
  • in males stimulates penile growth, spermatogenesis, prostate growth and function

therapeutic:
- intramuscular depot injections or patches used for replacement therapy in males (andropause), hypogonadism (pituitary or testicular disease) and female hyposexuality (ovariectomy)

*effects depend on age/sex of pt: development of male secondary characteristics in pre-pubertal men and masculinisation of women

40
Q

what is the therapeutical use of anti-androgens?

A

flutamide, cryptoterone:
-used as treatment of prostate cancer

dihydrotesterone synthesis inhibitors (finasteride):
- used in benign prostatic hypertrophy

41
Q

what are the effects of anabolic steroids?

A
  • modified androgens
  • increase protein synthesis and muscle development (e.g. nadrolone)
  • can be used in therapy of aplastic anaemia
  • SEs = infertility, salt and water retention, coronary heart disease and liver disease
42
Q

what are the effects of GnRH (decapeptide) analogues?

A
  • used to manipulate the reproductive axis
  • GONADORELIN (same aa seq) and NAFARELIN (more potent)
  • given in pulsatile fashion to stimulate the release of gonadotrophins (FSH and LH) induce ovulation (Rx of infertility)
  • given continuously will stimulate gonadal suppression. used in sex hormone-dependent conditions (e.g. prostate and breast cancer, endometriosis and large uterine fibroids)
43
Q

what is the effects of gonadotropin therapy?

A
  • used to treat infertility caused by a lack of ovulation as result of hypopituitarism following failure of Rx with CLOMIPHENE (pure oestrogen antagonist at hypothalamus)
  • used to treat men with infertility due to hypogonadotrophic hypogonadism
44
Q

what is meant by gravida and parity?

A 
gravida = total number of confirmed pregnancies
parity = number of pregnancies reaching viable gestation (including live and still births)
45
Q

what are the 4 clinically important bleeding patterns?

A
  1. scheduled bleeding: menstrual bleeding or withdrawal bleed whilst on combined oral contraception or HRT
  2. unstable bleeding:
    - frequent = >5 bleeding periods within reference period
    - infrequent = <3
    - prolonged = 1 or more bleeding episodes lasting 14 bleeding days or more
    - spotting = vaginal discharge containing blood (may not need sanitary protection)
    - breakthrough = unscheduled bleeding that occurs between menstrual periods (on contraception)
    - amenorrhoea = no bleeding or spotting days throughout 90day reference period
  3. bleeding episode = one or more consecutive days of bleeding, bounded by blood-free days
  4. reference period = a 90 day period of time during use of hormonal contraceptive method
46
Q

why should PMB need to be investigated?

A

rule out uterine cancer

47
Q

when should you refer someone with irregular bleeding to specialist?

A

URGENT: if by physical exam you suspect ascites +/or pelvic abdominal mass

RAPID ACCESS 2week referral: if pelvic mass is associated with other features of cancer (e.g. unexplained bleeding or weight loss)

ROUTINE:

  • if medication hasn’t worked. E.g. NSAIDs +/or tranexamic acid should be stopped if symptoms have not improved within 3 cycles
  • if complications are present. E.g. pressure symptoms - dyspareunia or pelvic pain or urinary symptoms - from large fibroids
  • if the pt requests surgical rather than medical management
  • anaemia, not responding to Rx and other causes have not be excluded
48
Q

what drugs could you consider while pt is awaiting Rx or referral?

A

tranexamic acid and NSAIDs

49
Q

how would you retrieve an endometrial biopsy and what endometrial thickness is a diagnosis of endometrial cancer likely in 7.3% of cases?

A
  • pipelle biopsy taken in light of USS

- 5mm

50
Q

define perimenopause

A

starts when cycle becomes irregular. transition into menopause. symptoms most severe (?)

51
Q

what lifestyle advice would you give to someone going through the menopause to help control symptoms?

A

encourage weight loss, alcohol cessation, avoid caffeine, add soya milk to diet and try black cohosh

52
Q

what is the best action to take when pt has diabetes and is obese?

A
  • gain advice from specialist regarding risk vs benefit (e.g. higher risk of thromboembolism)
  • optimise BP, check fasting lipid profile and use HRT patches instead of oral
53
Q

how would you manage short term symptoms of menopause?

A

vasomotor:

  • if uterus present -> oestrogen and progesterone HRT
  • if absent -> oestrogen only HRT

psychological:

  • if low mood -> HRT
  • if anxiety -> CBT
  • (no evidence SSRI or SNRI)

altered sexual function:
- testosterone supplements

urogenital atrophy:
- vaginal oestrogen (Vagifem = much less messy then oestrogen cream)

pt at risk of breast cancer:

  • SSRI (paroxetine, fluoxetine) traditionally used for anxiety and depression but some can improv hot flushes in some women
  • SERM (clonidine used for hot flushes)
54
Q

how would you mange long-term effects of HRT?

A

thromboembolism:

  • increased risk with oral HRT
  • not by transdermal
  • if high risk VTE or BMI >30 give transdermal HRT
  • if FHx of VTE or hereditary thrombophilia refer to haematologist before HRT

CVS disease:
- not contraindicated to HRT

T2DM:
- doesn’t affect blood glucose

Breast cancer:

  • oestrogen only HRT = no risk
  • combined HRT = increased risk

osteoporosis:
-HRT decreases fragility fractures

Dementia:
- unknown risk

Loss of muscle mass and strength:
- insufficient evidence

55
Q

what are the differential diagnosis’ of a pt experiencing “menopausal symptoms”

A

amenorrhea - pregnancy, PCOS, anorexia
irregular bleeding - anovulatory cycles, pathology (endometriosis, PCOS, fibroids, adenomyosis, cysts, malignancy)
hot flushes - endocrine, tumours, drugs
vaginal atrophy - trauma, infection

56
Q

define:

a) menorrhagia
b) dysmenorrhoea
c) oligomenorrhoea
d) primary amenorrhoea
e) secondary amenorrhoea
f) metrorrhagia
g) PMB
h) premenstrual syndrome

A

a) heavy menstrual bleeding 80ml/cycle
b) painful menstrual bleeding
c) infrequent periods >35days - 6months between bleeds
d) periods never star
e) periods stop >6months (not menopause)
F) periods out with the range 23-35 days, with a variability of 7 days between shortest and longest cycle
g) bleeding 1 year after menopause
h) psychological and physical symptoms in luteal phase

57
Q

what 3 questions should you ask yourself if a pt presents with amenorrhoea?

A

*diagnosis based on characteristics

1) is it primary or secondary?
2) is it pathological (disease process) or physical (normal for person? anorexia? pregnancy? menopause?)
3) location of problem site (think hypothalamus/ GnRH, pituitary/FSH+LH, ovaries, uterus, cervix or vagina. then think broader -> systemic problem eg anorexia. also think thymus, adrenals)

58
Q

what are the most common causes of primary and secondary amenorrhoea?

A

primary:

  • female triad: anorexia, psychological, athleticism
  • constitutional delay

secondary :

  • pregnancy, lactation, menopause
  • hyperprolacticaemia
  • PCOS
59
Q

how would you manage amenorrhoea?

A
  • Hx
  • examination: general, neuro, endocrine, pelvic
  • bloods (oestrogen, FSH, TSH, prolactin, pregnancy test, androgens) [e.g. low oestrogen and high FSH would suggest POI or early menopause. serum FSH/LH, oestrogen and prolactin will allow a distinction between primary gonadal and hypothalamic-pituitary causes]
  • imaging: consider TVUSS, MRI head

Rx:
• Refer if unknown Pathology
• Treat underlying cause
• treat the osteoporosis risk: diet, Vit D, calcium, COCP, HRT

60
Q

PCOS is the most common cause of ovarian dysfunction/amenorrhoea or oligomenorrhoea in practice .

a) what is the likely pc?
b) how is it defined?
c) what are the investigations?
d) what are the complications of PCOS?
e) what is the Rx?

A

a) amenorrhoea, oligomenorrhoea, w/gain, hirsutism (physical or clinical)
b) Defined by the presence of 2/3 of the following criteria: (i) oligo- and/or anovulation; (ii) hyperandrogenism; (iii) polycystic ovaries (USS), with the exclusion of other aetiologies.
e) increase in androgens. serum prolactin slightly raised. transvaginal USS revels pearl like ‘cysts’.
d) diabetes (T2), subfertility, gestational diabetes, metabolic syndrome. endometrial cancer (high levels of unopposed oestrogen)
e) weight loss! anti-androgens, oestrogens to reduce free androgens, contraceptive pill to regulate menstrual cycle

61
Q

why is diabetes a complication of PCOS?

A

increase in androgens –> increase in insulin resistance (T2DM) –> compensatory increases insulin –> increase androgens (vicious cycle)

*insulin resistance has a negative impact on the liver –> produces less SHBP –> less bound androgen –> more androgen effect

62
Q

what is the likely aetiology of menorrhagia?

A
  • most commonly it is idiopathic
  • 30% fibroids
  • 10% polyp
  • can have rare cause: hypothyroid, coagulopathy
63
Q

how would you investigate menorrhagia?

A

-Hx: ask a lot about the bleeding (clot, flooding, protection); the consequences like anaemia- SOB, fatigue, pallor; systemic symptoms - thyroid, coagulopathy; meds - anti-coagulants, hormonal contraceptives

exam:

  • speculum and bimanual looking for fibroids, adenomyosis
  • systemic disease and complications

Ix:

  • preg test
  • bloods: Hb, TFTs, clotting
  • pelvic TVUSS, endometrial biopsy, hysteroscopy
64
Q

how would you treat menorrhagia?

A

2 q’s to be answered:

  1. is your pt planning a pregnancy?
  2. is there an underlyin worrying pathology?
    - if answer to both is no 1st line Rx = intrauterine system (Mirena coil (progesterone)).
    - 2nd = combined pill
    - 3rd line (*or answer is yes) NSAIDs (mefenamic acid) and antifibrinolytics (tranexamic acid)
    - 4th line = GnRH analogues: chemical menopause
    - 5th = surgery (e.g. fibroid removal)
65
Q

fibroids are the most common cause of menorrhagia.

a) what is the likely PC?
b) what are the risk factors?
c) how would you Ix?
d) what is the Rx?

A

a) asymptomatic but can cause menorrhagia, also pelvic pn, dysmenorrhoea, pressure symptoms (e.g. on bladder freq + urgency), subfertility
b) black/Asian women, hereditary, reproductive years, early menarche, nulliparous
c) FBC, TVUSS
d) as per menorrhagia. refer if complications/failure to respond. red flags = acute pain, irregular bleeding, increase in size postmenopausal (bleed into fibroid or possible malignancy)

66
Q

describe the differences between primary and secondary dysmenorrhoea

A

primary:
- starts within 2 years of menarche (so will have for the rest of life)
- normal, not associated with abnormal pathology (increased prostoglandins in menstrual fluid)
- most severe on day 1 of bleed
- cramping lower abdo pn, radiates to lower back and legs +/- nausea, vomiting, fatigue, headache
- Rx = NSAIDs (reduce prostaglandins), COCP (stop ovulation), mirena coil (stop bleeding)

secondary;

  • occurs many ears after menarche
  • same symptoms but addition of deep dyspareunia! also starts in luteal phase and continues throughout menstruation
  • associated with pathology e.g. endometriosis!, chronic PID, fibroids, adenomyosis, polys (Ix= speculum, bimanual +/- TVUSS and laparoscopy)
  • Rx underlying cause and as per primary
67
Q

endometriosis is the most common cause of dysmenorrhoea. what is the:

a) pathophysiology?
b) clinical pres
c) clinical findings
d) management

A

a) presence of endometrial tissue out with the endometrium that responds to hormonal response -> bleed -> pain
b) severe dymenorrhoea, chronic pelvic pn, deep dyspareunia, ovulation pain, chronic fatigue, infertility
c) ‘chocolate cysts’, thickened nodular ligaments, fixed uterus, enlarged overt, tenderness
d) analgesics, combined or prog only contraceptives, GnRH analogues. surgical removal of cysts or hysterectomy

68
Q

name 3 d/D of menopausal symptoms?

A
  • PCOS
  • depression
  • thyroid dysfunction

week 23: irregular menstruation (1 decks)

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