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MSc Endocrinology > Investigation of Erectile Dysfunction and Amenorrhoea > Flashcards

Investigation of Erectile Dysfunction and Amenorrhoea Flashcards

1
Q

What is Menarche?

A

Age at first period

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2
Q

What is Oligomenorrhoea and Amenorrhoea?

A
  • Amenorrhoea: Complete absence of menstruation or cycle length >6 months
  • Oligomenorrhoea: Menstrual cycle length >6 weeks but <6 months
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3
Q

What is Primary and Secondary Amenorrhoea?

A
  • Primary Amenorrhoea: Failure to begin spontaneous menstruation by age 16
  • Secondary Amenorrhoea: Absence of menstruation for 3 months in a woman who has previously had cycles
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4
Q

What is Erectile Dysfunction?

A

Erectile dysfunction: Inability of the male to achieve or sustain an erection adequate for satisfactory intercourse

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5
Q

How is Gonadal function regulated?

A

Hypothalamic GnRH secreted

Pituitary LH & FSH secreted in response

Males

  • LH stimulates testosterone synthesis in Leydig cells
  • FSH stimulates spermatogenesis and synthesis of inhibin in Sertolli cells
  • Negative feedback of inhibin on FSH and of testosterone on GnRH

Females

  • LH & FSH (& follicular AMH) regulate E2 synthesis and oocyte maturation
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6
Q

What is the role of Kisspeptin Neurons?

A
  • Kisspeptin neurons may act as central processors for relaying signals from the periphery to GnRH neurons
  • Kisspeptins (Kiss1 gene) are secreted by neurons in discrete hypothalamic nuclei, directly innervating and stimulating GnRH neurons through GPR54 receptors (Kiss1r gene)
  • They are required for puberty and normal reproductive function. Kiss1 and Kiss1r mutations cause profound hypogonadotropic hypogonadism
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7
Q

How do Kisspeptin neurons regulate GnRH?

A
  • Kisspeptin neurons express E2 and androgen receptors and are direct targets for the action of gonadal steroids in males and females.
  • Kiss1 mRNA is both negatively and positively regulated by sex steroids
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8
Q

What are the roles of Kisspeptin signalling?

A
  • Negative feedback of sex steroids on gonadotropin secretion
  • Generation of preovulatory GnRH/LH surge
  • Triggering and guiding the tempo of sexual maturation at puberty
  • Controlling seasonal reproduction
  • Restraining reproductive activity during lactation
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9
Q

How is Kisspeptin signalling regulated?

A
  • Hypothalamic-pituitary-adrenal axis

Metabolic cues

  • Kiss1 may be induced by leptin

Environmental cues:

  • Time of day via suprachiasmatic nucleus (SCN) of the hypothalamus
  • Day length via melatonin from the pineal gland
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10
Q

How does Kisspeptin signalling take place in reproductive life?

A

Pulsatile GnRH stimulates pubertal LH & FSH release to causes gamete formation, gonadal steroid hormone production and feedback loops regulate GnRH, LH & FSH release

Kisspeptin neurons relay steroid feedback on GnRH

In Females: high oestrogen & progesterone levels

  • Stimulate kisspeptin neurons of the AVPV to induce the preovulatory surge of GnRH & LH
  • Inhibit Kiss1 expression in the arcuate nucleus (ARC)

In Males: High testosterone levels

  • Suppress GnRH, LH & FSH release, partly via kisspeptinneurons of the ARC
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11
Q

What are factors of the examination considered in the clinical assessment of amenorrhoea?

A
  • General health
  • Body shape and skeletal abnormalities
  • Weight and height
  • Hirsutism and acne
  • Evidence of virilization
  • Maturity of secondary sexual characteristics
  • Galactorrhoea
  • Normality of vagina, cervix and uterus
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12
Q

What is involved in the biochemical assessment of amenorrhoea?

A
  • LH, FSH & E2 (follicular ideally day 2-3)
  • Prolactin
  • Progesterone (day 21 or 7 days before expected bleed)
  • >30 nmol/L = ovulation
  • Testosterone, androstenedione, DHEAS & SHBG
  • 17-hydroxyprogesterone (basal + ACTH-stimulated)
  • Thyroid function tests
  • HCG
  • Steroid profiling
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13
Q

What are factors of the history considered in the clinical assessment of amenorrhoea?

A
  • Date of onset
  • Age of menarche, if any
  • Sudden or gradual onset
  • ? Pregnant
  • General health
  • Weight, absolute and changes in recent past
  • Stress (job, lifestyle, exams, relationships)
  • Excessive exercise
  • Drugs
  • Hirsutism, acne, virilization
  • Headaches/visual symptoms
  • Sense of smell
  • PMH of pregnancies
  • PMH of gynaecological surgery
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14
Q

What are some pituitary function tests?

A
  • GnRH test – investigation of gonadotrophin deficiency
  • Clomifene test
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15
Q

What is the GnRH test?

A
  • 100 µg intravenous GnRH
  • Samples at 0, 20, 60 min
  • Expect LH & FSH increase; post-pubertal LH rise > FSH rise (reverse if pre-pubertal LH rise < FSH rise)
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16
Q

What is the Clomifene test?

A
  • Selective oestrogen receptor modulator (SERM). Helps distinguish gonadotrophin deficiency from weight-related hypogonadism
  • 50 mg clomifene given for 5 days and LH & FSH measured on day 0 and 7
  • LH & FSH should increase to above reference range or 2x basal values
  • Lack of response suggests LH & FSH deficiency due to pituitary/hypothalamic disease
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17
Q

What are side effects of Clomifene test?

A
  • Depression
  • Visual disturbances
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18
Q

What are non-biochemical assessments of amenorrhoea?

A

Imaging:

  • MRI/CT scan
  • Ovarian/trans-vaginal ultrasound

Surgical:

  • Hysteroscopy
  • Laparoscopy
  • Biopsy
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19
Q

What are possible diagnoses of Primary Amenorrhoea?

A
  • Ovarian dysgenesis
  • Premature ovarian failure
  • Steroid biosynthetic defect
  • Oophorectomy
  • Chemotherapy
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20
Q

What are tests for Primary Amenorrhoea?

A
  • Karyotype
  • Ultrasound of ovary/uterus
  • Autoantibodies
  • Laparoscopy/biopsy of ovary
  • HCG stimulation
  • Urine steroid profiling
21
Q

What are biochemical tests for Primary Amenorrhoea?

A
  • LH↑
  • FSH↑
  • E2↓
  • PRL-
  • T-
22
Q

What are possible diagnoses for secondary/tertiary amenorrhoea?

A
  • Kallmann’s syndrome*
  • Hypothalamic amenorrhoea*
  • Weight-related amenorrhoea*
  • Exercise-induced amenorrhoea and anorexia*
  • Post-pill amenorrhoea
  • General illness*
  • Hyperprolactinaemia
23
Q

What are tests for causes of secondary/tertiary amenorrhoea?

A
  • TSH, free T4 & free T3
  • Prolactin
  • GnRH test
  • Clomifene test
  • Consider full pituitary screen
  • Pituitary MRI
24
Q

What are biochemical markers of secondary/tertiary amenorrhoea?

A
  • LH↓
  • FSH↓
  • E2↓
  • PRL-
  • T-
25
Q

What are possible diagnoses for hyperprolactinaemia related amenorrhoea?

A
  • Prolactinoma
  • Idiopathic hyperprolactinaemia
  • Hypothyroidism
  • Polycystic ovarian disease
  • Physiological in lactation
  • Dopamine antagonist drugs
26
Q

What are tests for hyperprolactinaemia related amenorrhoea?

A
  • Serum free T4/TSH
  • Other tests for PCOS
  • Pituitary MRI
  • (Macroprolactin)
27
Q

What are biochemical markers of Hyperprolactinaemia related Amenorrhoea?

A
  • LH ↓
  • FSH ↓
  • E2 ↓
  • PRL ↑ or ↑↑
  • T -
28
Q

What are biochemical markers for PCOS and Cushing’s syndrome?

A
  • LH: ↑/N
  • FSH: N
  • E2: N
  • PRL: N/↑
  • T: N/↑
29
Q

What are tests for PCOS and Cushing’s syndrome?

A

Polycystic Ovarian Syndrome

  • Androstenedione, DHEAS, cortisol

Cushing’s Syndrome (rarely)

  • SHBG
  • Ovarian ultrasound
30
Q

What are biochemical markers of androgen excess, gonadal or adrenal tumour, and congenital adrenal hyperplasia?

A
  • LH: N/↓
  • FSH: N/↓
  • E2: N/↓
  • PRL: N
  • T: ↑↑
31
Q

What are tests for adrogen excess, gonanal or adrenal tumur, and congential adrenal hyperplasia?

A
  • Androgen excess - Imaging ovary/adrenal
  • Gonadal or adrenal tumour - 17α-OH-progesterone
  • Congenital adrenal hyperplasia - Steroid profiling
32
Q

What are biochemical markers of Uterine/Vaginal abnormality, Imperforate hymen, absent uterus and lack of endometrium?

A
  • LH: N
  • FSH: N
  • E2: N
  • PRL: N
  • T: N
33
Q

What are tests Uterine/vaginal abnormality, Imperforate hymen, Absent uterus, Lack of endometrium?

A
  • Uterine/vaginal abnormality - Examination findings
  • Imperforate hymen* - Ultrasound of pelvis
  • Absent uterus* - Progesterone challenge
  • Lack of endometrium - Hysteroscopy
34
Q

How is Amenorrhoea treated?

A
  • Treat underlying pathology if possible
  • Lifestyle management
  • Oestrogen replacement
35
Q

What is Menopause?

A
  • Cessation of menstruation at the end of a woman’s reproductive life
  • Mean age of the menopause in the UK is about 53 years and average female life expectancy is 81 years
  • A woman may thus spend nearly 40% of her life in an oestrogen-deficient state
  • Premature menopause/ovarian failure defined as <40 years
  • Hypergonadotrophic hypogonadism (↑↑↑ FSH & LH, ↓ E2)
36
Q

What are symptoms of Menopause?

A
  • Headaches and Hot flashes
  • Teeth loose and Gums recede
  • Breast droop and flatten
  • Weight Gain and Abdomen loses muscle tone
  • Backaches
  • Vaginal dryness/itching
  • Bones lose mass and more fragile
37
Q

How is menopause diagnosised and managed?

A

Clinical diagnosis in women aged > 45 years:

  • Perimenopause if vasomotor symptoms and irregular periods
  • Menopause if 12 months no period and no hormonal contraception

Do NOT use FSH testing:

  • In women aged > 45 years
  • If combined contraception/high-dose progestogen

Do consider FSH if <40 years (? premature)

Do consider FSH if aged 40-45 with symptoms

38
Q

What is Erectile dysfunction?

A
  • Inability of the male to achieve or sustain an erection adequate for satisfactory intercourse
39
Q

What are congenital casues of Erectile Dysfunction?

A
  • Anorchia/Leydig cell agenesis
  • Cryptorchidism (testicular maldescent)
  • Chromosome abnormality (e.g. Klinefelter’s syndrome)
  • Enzyme defects: 5α-reductase deficiency
  • Androgen receptor deficiency/abnormality
  • Sickle cell disease
40
Q

What are acquired causes of Erectile Dysfunction?

A
  • Testicular torsion
  • Orchidectomy
  • Local testicular disease
  • Chemotherapy/radiation toxicity
  • Orchitis (e.g. mumps)
  • Chronic kidney disease
  • Cirrhosis/alcohol
  • Infections – STI
  • Autoimmune
41
Q

What are causes of secondary (pituitary) / tertiary (hypothalamic) erectile dysfunction?

A
  • Reduced gonadotrophins (Hypopituitarism)
  • Selective gonadotrophic deficiency (Kallmann’s syndrome)
  • Normosmic idiopathic hypogonadotropic hypogonadism
  • Severe systemic illness
  • Severely underweight
  • Hyperprolactinaemia
42
Q
A
  • Diuretics: Thiazides (e.g. bendroflumethiazide), spironolactone
  • Anti-hypertensives: Methyldopa, clonidine, beta-blockers (e.g. propranolol), verapamil
  • Fibrates: Clofibrate, gemfibrozil
  • Antipsychotics: Phenothiazines (e.g. chlorpromazine), butyrophenones (e.g. haloperidol)
  • Antidepressants: Tricyclics (e.g. amitriptyline), monoamine oxidase inhibitors (e.g. phenelzine), selective serotonin reuptake inhibitors (e.g. fluoxetine), lithium
  • H2-antagonists: Cimetidine, ranitidine
  • Hormones and hormone-modifying drugs: Oestrogens (e.g. estradiol), progesterone, corticosteroids (e.g. prednisolone), cyproteroneacetate, 5-alpha reductase inhibitors (e.g. finasteride)
  • Cytotoxics: Cyclophosphamide, methotrexate
  • Anti-arrhythmics and anticonvulsants: Disopyramide
43
Q

How is Erectile dysfunction investigated?

A
  • Fasting glucose / HbA1c (diabetic neuropathy)
  • Semen analysis
  • WHO/Kruger classification
  • Karyotyping
  • MRI/CT scan of pituitary
  • USS of testes
  • Testicular biopsy
  • Laboratory
44
Q

What are biochemical investigations of ED?

A
  • Testosterone/SHBG (9 am)
  • LH/FSH/E2
  • Prolactin
  • 17-OHP
  • TFTs
  • GGT/MCV/U&E
  • (Seminal fluid fructose and zinc)
  • Pituitary function tests
  • GnRH test
  • Clomifene citrate test (oestrogen antagonist)
  • HCG stimulation test
45
Q

What is the HCG stimulation test?

A
  • 2000 IU HCG given on days 0 and 2
  • Measure serum testosterone on days 0, 2 and 4.
  • Normal response testosterone increases above normal RR
  • No rise in testosterone indicates absence of functional testicular tissue

Useful if you think there is disrupted orchidogenesis

46
Q

How is testosterone transported?

A

Testosterone and dihydrotestosterone circulate in plasma

  • Unbound (‘free’) ~2–3% = biologically active
  • Bound to non-specific proteins e.g. albumin = biologically available
  • Bound to SHBG = biologically inactive
47
Q

How can testosterone be measured?

A

Can be measured - technically difficult!

  • Free testosterone assay measures unbound fraction
  • Bioavailable testosterone includes free plus weakly bound to albumin

Can also be calculated

48
Q

How is Erectile dysfucntion managed?

A

Counselling/Lifestyle

Medical

  • DM/Cardiovascular disease - control
  • PDE 5 inhibitor e.g. viagra (1st line treatment)
  • Intracavernous injection (2nd line treatment)
  • Penile implant (3rd line treatment)
  • Testosterone: Supraphysiological replacement has a negative effect on spermatogenesis
  • HCG: Hypogonadotrophic hypogonadism, intramuscularly twice weekly
  • Dopamine agonists: Hyperprolactinaemia, with dopamine agonists

High-dose corticosteroids – used in patients with sperm autoantibodies (side effects!)

Surgery

49
Q

What is Andropause?

A
  • Age related testicular failure
  • Poorly defined
  • Decreased bioavailable testosterone due to increasing SHBG
  • FSH tends to increase more with age than LH
  • Gynaecomastia increases with age

MSc Endocrinology (16 decks)

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