Male Hypogonadism & Gynaecomastia Flashcards

1
Q

Describe the male HPG axis

A

Kisspeptin stimulates the hypothalamus

The hypothalamus releases GnRH

The anterior pituitary releases FSH & LH

The testes release testosterone

Testosterone negatively feedbacks to the hypothalamus & pituitary gland

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2
Q

Where is testosterone produced and which hormone controls this?

A

Testosterone is produced by Leydig cells under the control of LH.

The synthesis of LH is controlled by negative feedback mechanisms of testosterone

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3
Q

Which hormone acts on Sertoli cells?
What protein is produced by Sertoli cells?
What is the role of these cells in the negative feedback of the male HPG axis?

A

FSH acts on Sertoli cells
Sertoli cells produce androgen binding protein.
They also produce inhibin which negatively feedbacks on the hypothalamus/pituitary gland

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4
Q

What is the other name for a) primary hypogonadism b) secondary hypogonadism

A

A) primary hypogonadism aka hypergonadotrophic hypogonadism - testicular failure

B) secondary hypogonadism aka hypogonadotrophic hypogonadism - hypothalamic/ pituitary cause

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5
Q

State the effect of hypergonadotrophic hypogonadism and hypogonadotrophic hypogonadism on a) spermatogenesis b) testosterone production.

A

Hypergonadotrophic hypogonadism
- Spermatogenesis affected > testosterone production

Hypogonadotrophic hypogonadism
- Spermatogenesis affected = testosterone production

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6
Q

hypergonadotrophic hypogonadism aetiology

A
  • Vascular e.g. varicocele
  • Infections (orchitis) e.g. mumps
  • Drugs e.g. corticosteroids, ketoconazole
  • Iatrogenic e.g. Chemotherapy/radiation
  • Congenital e.g. Klinefelter’s syndrome
  • Trauma e.g. Testicular torsion
  • Metabolic/Infiltrative e.g. haemochromatosis
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7
Q

Describe the genetics of Klinefelter’s syndrome

A

NOT inherited
Caused by non-disjunction
Usually 47 XXY

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8
Q

Klinefelter’s syndrome presentation

A
  • Infertility (tubular damage)
  • cryptorchidism, small testicular size
  • learning disability, psychological effects
  • Increased risk of breast & non-Hodgkin lymphoma
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9
Q

Klinefelter’s syndrome investigations

A

Diagnosed by karyotyping

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10
Q

Hypogonadotrophic hypogonadism

A
  • Infection e.g. TB
  • Neoplasm e.g. pituitary tumour
  • Drugs e.g. Corticosteroids, opioids
  • Congenital e.g. kallmann’s syndrome
  • Trauma e.g. head trauma, pituitary damage
  • Endocrine e.g. hyperprolactinaemia
  • Other conditions - Eating disorders, excessive exercise, obesity, diabetes
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11
Q

Describe Kallmann’s syndrome

A

Genetic disorder (mutation) that causes hypogonadotropic hypogonadism and an impaired sense of smell (asomnia).

Diagnosed by hormone, olfactory function & genetic testing. Treated with HRT

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12
Q

Hypogonadism presentation (pre-pubertal)

A

DIFFERENT
- Small male sexual organs (testes, penis, prostate)
- high-pitched voice
- ‘Eunuchoidal’ habitus (tall, slim, long arms and legs)

SAME
- Decreased body hair, low libido
- Gynaecomastia
- Decreased bone and muscle mass
- +/- symptoms due to cause (e.g. asomnia with Kallmann’s syndrome)

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13
Q

Hypogonadism presentation (post-pubertal)

A
  • Normal skeletal proportions, penis/prostate size and voice
  • Decreased energy and motivation
  • Decreased testicular volume
  • Decreased libido, decreased spontaneous erections
  • Decreased pubic/axillary hair, reduced shaving frequency
  • Gynaecomastia
  • Decreased muscle and bone mass
  • +/- symptoms due to cause (e.g. pituitary lesion causing visual field defect)
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14
Q

Hypogonadism investigations

A
  • 9am testosterone (repeat x2, 2 weeks apart)
    • hypogonadism diagnosis
  • LH/FSH test
    • hyper vs hypo gonadotrophic differentiate
  • Aetiology specific tests
    • e.g. MRI, karyotyping, iron studies, prolactin levels…
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15
Q

Why is both SHBG & total testosterone measured & ‘free testosterone’ calculated when measuring testosterone levels?

A
  • A portion of testosterone is bound to SHBG,
  • making it not ‘free’ or active.
  • SHBG levels vary between individuals
  • Total testosterone includes the SHBG-bound testosterone
  • Therefore SHBG must also be measured
  • To calculate an accurate ‘free testosterone’ level
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16
Q

Hypogonadism treatment

A

If fertility is important
- GnRH or LH/FSH therapy OR
- Sperm donor

If not
- Testosterone replacement therapy (gel/capsule/IM)

17
Q

Testosterone replacement therapy contraindications

A
  • Hormone responsive cancer e.g. prostate/ breast (history/current/possible diagnosis)
  • Haematocrit > 50%
  • Severe OSA or HF
18
Q

Testosterone replacement therapy monitoring

A
  • Testosterone levels
  • Prostate cancer screening
  • Haematocrit levels
  • OSA symptom monitoring
19
Q

State the two fates of testosterone and state the effects of these two molecules

A

1) Dihydrotestosterone (highly active form)

  • Sebum production
  • Prostate growth & enlargement
  • Effects on skin, hair follicles & external genitalia

2) Oestrogen

  • Epiphyseal fusion
  • Bone mass
  • Certain sexual behaviours
  • Verbal memory
  • Plasma lipids
20
Q

Where are Leydig & Sertoli cells located?

A

Leydig - Interstitial tissue between seminiferous tubules
Sertoli - Seminiferous tubules

21
Q

Gynaecomastia definition

A

Condition by whichmales develop breast tissuedue to animbalanced ratioof oestrogen and androgen activity

22
Q

Gynaecomastia aetiology

A

Physiological
- adolescence, delayed testosterone surge relative to oestrogen at puberty
- older population, decreasing testosterone with age

Pathological
- lack of testosterone (Klinefelter’s syndrome, androgen insensitivity, testicular atrophy, or renal disease)
- increased oestrogen (liver disease, hyperthyroidism, obesity, adrenal tumours, or certain testicular tumours)
- medications (digoxin, metronidazole, spironolactone, chemo, goserelin, antipsychotics, or anabolic steroids)

23
Q

Gynaecomastia investigations

A
  • Only if cause is unknown
  • Triple assessment if suspicion of malignancy
  • LFTs, U&E’s & then LH & testosterone if cause unknown

** Then management is tailored to the cause