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Endocrinology > eek 5 > Flashcards

eek 5 Flashcards

1
Q

range of normal menstrual cycle? menses length

A

21-35days

3-8days

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2
Q

when does ovulation usually occur in normal menstrual cycle? how much blood is normally lost?

A

day 14

30ml

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3
Q

what is menarche

A

when periods start

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4
Q

what are the three stages of ovarian cycle?

A

follicular, ovulation, luteal

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5
Q

what are the oestrogen levels when follicular stage begins/why does it occur?

A

low (oestrogen)

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6
Q

what stimulates follicle to develop?

A

Anterior pituitary secretes FSH and LH [stimulation follicle to develop]

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7
Q

what happens in development of follicle/follicular stage?

A
  • A leading follicle develops
  • Granulosa cells around egg enlarge, releasing estrogen
  • This causes this uterine lining to thicken

[BASICALLY:During this phase, the ovarian follicles mature and get ready to release an egg]

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8
Q

what are the stages of the uterine cycle?

A

menses, proliferative, secretory

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9
Q

why does ovulation occur?

A

Happens at the peak of follicular growth in response to LH surge

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10
Q

what happens in ovulation?

A

[BASICALLY:second phase of the ovarian cycle in which a mature egg is released from the ovarian follicles into the oviduct]

  • levels of estradiol reduce
  • massive LH peak (positive feedback mechanism due to prolonged exposure to estradoil)
  • proteolytic enzymes and prostaglandins are activated, → digestion of the follicle wall collagen → Follicle ruptures, releasing ova into the Fallopian tubes.
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11
Q

what is the luteal phase?

A

final phase of the ovarian cycle and it corresponds to the secretory phase of the uterine cycle; the lining of uterus gets thicker to prepare for a possible pregnancy

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12
Q

what is a corpus luteum?

A

It is the remains of the ovarian follicle that has released a mature ovum during a previous ovulation.

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13
Q

what does the corpus luteum do?

A

produce high levels of progesterone (peak at 1 week post-ovulation)

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14
Q

what happens to the corpus luteum

A

if pregnant - embryo will release hormones to preserve corpus luteum

if non-pregnant - stops progesterone, decays, uterine lining detaches, expelled by menstruation

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15
Q

what is expelled in menstruation? how long does this take?

A

Tissue, blood, unfertilized egg all discharged

Can take from 3-7 days

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16
Q

what is the HPO (hypothalamus-pituitary-ovary axis) hormones?

A

GnRH (Gonadotropin-releasing hormone) stimulates follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from ant pit.

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17
Q

what part of the hypothalamus is responsible for producing GnRH?

A

Arcuate nucleus

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18
Q

there are two parts of the ovary (outer cortex and inner medulla), which contains follicles?

A

outer cortex

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19
Q

what attaches the ovaries tot the pelvic wall?

A

the IP ligament [suspensory ligament of the ovary, also infundibulopelvic ligament]

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20
Q

what is the endometrium? what increases its thickness?

A

basal layer and superfuical layer of uterus (thickens in response to oestrogen)

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21
Q

what cause the endometrium to slough off?

A

Lack of hCG and progesterone

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22
Q

what is GnRH?

A
  • gonadotropin releasing hormone

- is a deca peptide hormones

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23
Q

how many types of GnRH are there? which important?

A

3 types of GnRH hormone

GnRH 1 is responsible for the reproductive function (released in pulsatile manner, t1/2=2-4mins)

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24
Q

what is FSH?

A
  • follicle-stimulating hormone

- glycoprotein, t1/2 - hours

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25
Q

why is FSH important?

A

responsible for recruiting the dominant follicle

It is also responsible for granulosa cell growth and activates aromatase activity (precursor to oestrogen)

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26
Q

what does LH do?

A
  • Acts on the theca cells
  • Uptake of cholesterol
  • Androgens to oestrogens
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27
Q

what does oestrogen do?

A

Acts synergistically with FSH

Induces FSH and LH receptors

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28
Q

where are inhibins found?

A

[Local peptide] in the follicular fluid

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29
Q

what do inhibins do?

A

-ve feed back on pituitary FSH secretion

Locally enhances LH-induced androstenedione production

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30
Q

where are activins found? what do they do?

A

Found in follicular fluid

Stimulates FSH induced estrogen production

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31
Q

what are the tubular components of the testes?

A

sertoli cells

germ cells

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32
Q

what are the interstitial components of the testes

A

Leydig cells

Capillaries

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33
Q

what is the function of sertoli cells? how do they do this?

A

to support germ cells in development

in sperm maturation, excess cytoplasm and materials in the cells are “eaten up” by Sertoli cells,

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34
Q

what is the function of germ cells?

A

to mature into sperm

[Spermatogonia → 1° Spermatocytes
→2° Spermatocytes
→Spermatids (Early to Elongated)
→Testicular spermatozoa]

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35
Q

what occurs in the maturation of sperm?

A

formation of acrosome from Golgi(digestive enzymes) - outer shell for ovum

formation of flagellum from centriole - tail for motility

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36
Q

why is egg bigger than ovum? (what does it contain that sperm doesn’t )

A 
yolk proteins
ribosomes
t-RNA
m-RNA
protective chemicals

(cytoplasm and organelles necessary for cell division and growth to begin)

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37
Q

site of fertilisation?

A

ampulla of the fallopian tube

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38
Q

what are pre-fertilisation events that occur in women?

A

thinner cervical mucus

fibril end comes into contact with ovary and peristalsis brings egg to ampulla

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39
Q

what is Capacitation

A

functional maturation of the spermatozoon

necessary for acrosome reaction (enzyme to penetrate egg)

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40
Q

process of fertilisation

A

chemotaxis, release of acrosomal enzymes, binding of sperm, passage through extracellular envelope, fusion of pronuclei

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41
Q

chemotaxis in fertilisation

A

Around the egg there are specific receptors that produces exocytosis and acrosome reaction

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42
Q

what triggers please of acrosomal enzymes?

A

Zona pellucida ZP3 [when sperm comes in contact with egg]

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43
Q

what occurs in the binding of sperm in fertilisation?

A

corona radiata (part of ovum) broken through (aided by flagellum), bona reaction then occurs preventing polyspermy

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44
Q

how is polyspermy avoided?

A

fast block (NA+ influx changes membrane potential)

slow block (kinase stimulation has many effects, e.g.: inc calcium)

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45
Q

what occurs in egg activation?

A

Dramatic increase in the levels of free intracellular Ca2+ ions in the egg shortly after the sperm makes contact with the egg’s plasma membrane

Act as second messengers to initiate changes

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46
Q

what does sperm penetration do?

A
  • inc Ca2+
  • triggers egg to complete meiosis
  • triggers cytoplasmic rearrangement
  • sharp inc in protein synthesis and general metabolism
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47
Q

fusion of nuclei in fertilisation

A

final stage of fertilisation; haploid sperm and egg fuse for diploid zygote

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48
Q

where is oestrogen produced in the body?

A

ovaries, adrenal glands and fatty tissue

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49
Q

how is oestrogen made?

A

aromatase acts on steroid precursors creating estradiol

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50
Q

why do fat men get ED?

A

inc fat means inc oestrogen and this decreases testosterone = ED (also neurological/vascular problems at higher risk)

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51
Q

what is Oligomenorrhea

A

reduction in frequency of periods to less than 9/year

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52
Q

what is Primary amenorrhea

A

failure of menarche by the age of 16 years

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53
Q

what is Secondary amenorrhea

A

cessation of periods for >6 months in an individual who has previously menstruated

54
Q

what are causes of amenorrhea?

A

physiological,

primary and secondary amenorrhea

55
Q

what are physiological causes of amenorrhea?

A

Pregnancy

Post-menopausal

56
Q

causes of Primary amenorrhea

A

Consider congenital problems (Turner’s syndrome, Kallman’s syndrome), anatomical problem

57
Q

causes of secondary amenorrhea?

A

Ovarian problem: PCOS, Premature Ovarian Failure

Uterine problem: uterine adhesions

Hypothalamic Dysfunction: weight loss, over exercise, stress, infiltrative

Pituitary: high PRL, hypopituitarism

58
Q

Hx of amenhorrhea

A

Symptoms of oestrogen deficiency (flushing, libido, dyspareunia)

Hypothalamic problem: exercise, weight loss, stress

Features of PCOS/androgen excess : hirsutism/acne

Anosmia ?Kallman’s

Symptoms of hypopituitarism/pituitary tumour including galactorrhea

?Drugs associated with hyperprolactinemia

59
Q

Examination of amenorrhea

A

Body habitus ?Turners
Visual fields/anosmia
Breast development
Hirsutism/acne/androgen excess

60
Q

investigating oligo/amenorrhea (necessary )

A
  • LH, FSH, Oestradiol

- Thyroid function, Prolactin

61
Q

what additions investigation can be done for oligo/amenorrhea

A

Ovarian ultrasound +/- endometrial thickness
Testosterone if hirsutism
Pituitary function tests + MRI pituitary if hypothalamic pituitary probems suspected
Karyotype if primary amenorrhea or features of Turner’s syndrome

62
Q

what is female hypogonadism identified by?

A

low levels of oestrogen

63
Q

why when body is under stress (phycological, anorexia, exercise…) do periods stop?

A

body stops GnRH (as doesn’t want to get pregnant when not well)

64
Q

a low estradiol and low FSH/LH diagnose what?

A

secondary hypogondism

65
Q

a low estradiol and high FSH/LH diagnose what?

A

primary hypogonadism (ovaries have packed up)

66
Q

where is cholesterol converted to oestrogen?

A

in the ovaries (primarily) - deficiency leads to amenhorrea

67
Q

what is primary hypogonadism also known as?

A

hypergonadotrophic hypogonadism

68
Q

what is secondary hypogonadism also known as?

A

hypogonadotrophic hypogonadism

69
Q

commonest cause of primary hypogonadism

A

premature ovarian failure

70
Q

commonest causes of secondary hypogonadism?

A

high PRL, hypopituitarism (primary pit or hypothalmic problem)

71
Q

what is premature ovarian failure (POF) classified as?

A

loss of normal function of your ovaries before age 40(early menopause)

72
Q

what is POF

A

Amenorrhea, oestrogen deficiency and elevated gonadotrophins occuring < 40years of age, as a result of loss of ovarian function

73
Q

how is POF diagnosed?

A

FSH >30 on 2 separate occasions > 1 month apart

74
Q

causes of POF

A
  • Chromosomal abnormalities (e.g. Turner’s syndrome, Fragile X)
  • Gene mutations (e.g. FSH receptor/LH receptor)
  • Autoimmune disease (e.g. association with Addison’s, thyroid, APS1/2)
  • Iatrogenic (radiotherapy/chemotherapy)
75
Q

what is Secondary Hypogonadism?

A

Hypogonadism as a result of hypothalamic or pituitary disease
Characterised by low oestradiol with low/normal LH/FSH

76
Q

causes of Secondary Hypogonadism?

A

Hypothalamic problem:
Functional hypothalamic disorders
Kallman’s syndrome
Idiopathic hypogonadotrophic hypogonadism (IHH)

Pituitary problems

Miscellaneous:
Prader-Willi
Haemachromatosis

77
Q

functional hypothalamic amenorrhea (factors affecting)

A

Weight change
Stress
Exercise

Anabolic steroids
Systemic illness
Iatrogenic (surgery/radiotherapy)
Recreational drugs
Head Trauma
Infiltrative disorders e.g sarcoidosis
78
Q

what is Idiopathic hypogonadotrophic hypogonadism (IHH)?

A

Identified by absent or delayed sexual development associated with inappropriate low levels of gonadotrophin and sex hormone levels in absence of anatomical / functional defects of hypothalamic-pituitary gonadal axis

79
Q

features of Idiopathic hypogonadotrophic hypogonadism (IHH)?

A

inability to activate pulsatile GnRH

-hypogonadism, e.g: reduced or absent puberty, low libido, infertility,

80
Q

hats the role of kisspeptin in regulation of GnRH?

A

the ligand for KISS1R – ‘Kisspeptin’ - is a potent stimulator of GnRH secretion

81
Q

what is Kallman’s syndrome?

A

A genetic disorder characterised by a loss of GnRH secretion + anosmia or hyposmia; rest of pituitary function normal

82
Q

how is kallman’s syndrome diagnosed?

A

clinical diagnosis of exclusion (MRI normal as is only absence of olfactory bulbs); FHx association.

83
Q

what is difference between klaxon’s syndrome and IHH?

A

kallamans is a form of HH (has smell deficit)

84
Q

pituitary dysfunction investigations relating to

A

loss of LH/FSH stimulation

hyperprolactinemia

85
Q

causes of loss of LH/FSH (pituitary dysfunction )

A

Non-functioning pituitary macroadenoma (pressure effects lead to hypopituitarism)

Empty Sella

Pituitary infarction

86
Q

cause of hyperprolactinemia

A 
Prolactinomas
Other pituitary pathology
Drugs (anti-psynchotics, dopamine antagonists)
Hypothyroidism
Idiopathic
87
Q

what are the ovarian causes of amenorrhea?

A

PCOS
ovarian failure (high gonadotrophins)
congenital problem

88
Q

what are the criteria for diagnosing PCOS?

A

normal oestrogen levels

2/3: menstrual irregularity, Hyperandrogenism (hirsutism, elevated free testosterone)
Polycystic ovaries

89
Q

what congenital problems can cause amenorrhea?

A

(Absence of Uterus, Vaginal atresia)

Turner Syndrome, Testicular feminisation, congenital adrenal hyperplasia (late onset CAH)

90
Q

what is hirsutism?

A

excess hair; usually used when referring to women with male pattern hair distribution

91
Q

why does hirsutism occur?

A

Caused by androgen excess at the hair follicle:

  • Due to excess circulating androgen
  • Due to increased peripheral conversion at the hair follicle
92
Q

what does PCOS stand for?

A

Polycystic Ovarian Syndrome

93
Q

causes of hirsutism?

A

PCOS (commonest)
Familial, idiopathic, non-classical congenial adrenal hyperplasia
adrenal/ovarian tumour

94
Q

what are signs of worrying hirsutism? what is cause?

A

short Hx, sign of virilisation,

due to Adrenal or Ovarian Tumour

95
Q

what is congenital adrenal hyperplasia (CAH)?

A

CAH is an inherited group of disorders characterized by a deficiency in one of the enzymes necessary for cortisol synthesis

96
Q

what are most CADs due to? genetics and PC?

A

90% due to 21α-hydroxylase deficiency, autosomal recessive with varied clinical presentation

97
Q

what are the two type of CAH? what is the difference?

A

classic CAH - typically diagnosed in infancy (e.g. virilisation/salt-wasting)

non-classic CAH - partial 21α-hydroxylase deficiency, Presents in adolescence/aduthood with hirsutism, menstrual distrbance, infertility due to anovulation

98
Q

what is turner’s syndrome?

A

45X0

99
Q

investigation of CAH [due to 21-OH deficiency] results

A

Increased 17-OH progesterone esp after ACTH stimulation

Synacthen test

100
Q

androgen-secrting tumours PC

A

rapid symptoms - virlisation, high testosterone levels

101
Q

androgen-secrting tumours investigation

A

MRI adrenals and ovaries will demonstrate tumours > 1cm

102
Q

PCOS treatment

A

metformin (high BMI)
oral contraceptive pill (regulates cycle, decreases ovarian androgens)
Anti-androgens (cyproterone acetate)
local anti-androgens (efflornithine cream)
cosmesis (laser phototherapy/electrolysis)

103
Q

treatment for late onset CAH?

A

Low dose glucocorticoid to suppress ACTH drive

104
Q

turner’s syndrome genetics

A

severe or mosaicism possible (only affects women, infertile)

105
Q

turner’s syndrome PC

A

short stature, webbed neck, shield chest with wide spaced nipples, underdeveloped breasts, Cubitus values, no menstruation

106
Q

turner’s syndrome PC in paediatrics

A

Short Stature
Failure to progress through puberty:
-Normal adrenarche (pubic hair development)
-Breast development – depends when ovaries fail. May have no breast development
- 30% have some pubertal development

107
Q

turner’s syndrome PC in adults

A

Primary or secondary amenorrhea

Infertility

108
Q

problems with CVS, GI and other

A

CVS:Coarctation of the aorta
Bicuspid aortic valve
Hypoplastic left heart

GI:Bleed (vascular malformation)
Increased Crohns/UC

Other: lymphoedema, AI hypothyroidism, osteoporosis, scoliois, otitis media, renal abnormalities

109
Q

rarer causes of amenorrhea

A

XX gonadal dysgenesis: absent ovaries but no chromosomal abnormality

Testicular feminisation/Androgen insensitivity syndrome: Genetically XY Male (with testes), but in the complete form, phenotypically female (pseudohermaphrodites)

110
Q

male hypogonadism PC

A

not enough testosterone

delayed puberty, reduced body hair and beard, enlarged breasts, loss of muscle, and sexual difficulties.

111
Q

what are the two types of male hypogonadism? what biochemical results seen?

A

Primary hypogonadism:
Low testosterone with high LH/FSH= Acquired and congenital causes

Secondary hypogonadism:
Low testosterone with inappropriate low LH/FSH = Pituitary /Hypothalamic disease

112
Q

causes of primary male hypogonadism?

A

kleinfelter’s, y-chromosome micro deletions, Undescended testicles, Hemochromatosis, Injury to the testicles/torsion, cancer treatment (irradition/chemo), orchitis (mumps)

113
Q

causes of secondary male hypogonadism?

A

hyperprolactinamiea, IHH (Kallmann syndrome). Pituitary disorders/damage. prader-willi syndrome, Inflammatory disease. medications, obesity

114
Q

Hx of male hypogonadism

A

Symptoms:
Sexual function (libido, erections, ejaculation)
Age of puberty, shaving frequency etc
Fertility
Symptoms of pituitary disease
Duration of symptoms/features (permanent vs acquired)

Other relevant history (trauma, infection, chemo/radiotherapy etc)

Signs
Staging of puberty (secondary sexual characteristics)
Testicular volume
Visual fields / other pituitary disease

115
Q

investigating hypogonadism in men

A

testosterone low, then measure LH/FSH. (high=primary and low=secondary hypogonadism)

116
Q

what is kleinfelter’s syndrome?

A

XXY (most common congenital form of primary hypogonadism)

117
Q

clinical features of kleinfelters?

A 
Reduced testicular volume
Gynaecomastia
Eunuchoidism
(intellectual dysfucntion in 40%)
(azoospermia)
118
Q

investigating kleinfelters

A

Low testosterone, high LH/FSH (elevated SHBG/oestradiol)

do Karytope: 47 XXY (or mosaicism)

119
Q

treatment of hypogonadism

A

consider testosterone replacement (young men)

[does not restore fertility]

120
Q

testosterone replacement pros

A

Improved sexual function
Bone health improved (BMD)
reduce fat and inc strength

121
Q

testosterone replacement cons

A

CVS risk

122
Q

secondary hypogonadism: generally case by and how is diagnosed?

A

Hypogonadism as a result of hypothalamic or pituitary dysfunction
Low 9am testosterone, low normal LH/FSH

123
Q

causes of secondary hypogonadism

A

congenital = IHH (inc kallman’s) + CAD

functional = exercise, weight change, stress, systemic illness
Infiltrative disorders – sarcoid, haemachromatosis,
Cranial irradiation / trauma
Drugs (e.g. anabolic steroids, opiates)
Hyperprolactinaemia
Hypothalamic or Pituitary tumours / surgery
Prader-Willi syndrome

124
Q

what is Gynaecomastia caused by?

A

Increased oestrogen action on breast tissue

125
Q

causes of Gynaecomastia

A

Physiological
Drugs: Oestrogens, testosterone, spironolactone, digoxin +many more
Hypogonadism
Tumours; Oestrogen/androgen testicular or adrenal origin; hCG secreting (e.g. germinoma)
Endocrine disorders (e.g. thyrotoxicosis, Cushings)
Systemic illness
Hereditary disorders

126
Q

Hx of Gynaecomastia

A 
Duration of symptoms
Pain?
Symptoms of hypogonadism
Symptoms of systemic disease
History of recreational drugs / alcohol
127
Q

exam of gynaecomastia

A 
Breast tissue vs fat
Unilateral/symmetrical
Any hard irregular nodules
Examination of testes ?tumour
General examination (e.g. ?liver disease)
128
Q

investigations and imaging of gynaecomastia

A

investigations = Testosterone, LH, FSH, Oestradiol, Prolactin, AFP, HCG, LFTs, SHBG

imaging = Breast imaging
Testicular/adrenal imaging

129
Q

treatment of gynaecomastia

A

Reassurance in majortiy of cases

Address underlying cause (e.g. remove causative drugs)

Surgery (cosmetic)
Medication (e.g. anti-oestrogens)

130
Q

what is infertility classed as?

A

failure to achieve a clinical pregnancy after 12 months of more of regular unprotected sexual intercourse (in absence of known reason) in a couple who have never had a child (WHO definition)

131
Q

what are the two types of infertility?

A

Either primary (couple never conceived) or secondary (couple previously conceived, although pregnancy may not have been successful e.g. miscarriage or ectopic pregnancy)

132
Q

factors affecting a woman’s fertility

A

<30, previous pregnancy, short time trying to conceive, intercourse around ovulation. BMI of 18.5-30kg/m2, non-smokering partners, no recreational drugs, limited caffeine.

Endocrinology (7 decks)

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