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MD1 endocrinologie > Les testicules > Flashcards

Les testicules Flashcards

1
Q

What is the normal size of an adult testicle?

A

Volume –> 18.6 ± 4.8 mL

Length –> 4.6 cm (3.6-5.5)

Width –> 2.6 cm (2.1-3.2)

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2
Q

What are the 3 layers surrounding the testicles?

A
  1. Vaginal
  2. Albuginea
  3. Vascular
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3
Q

Anatomical location of testes:

A

Start –> near kidneys

Start descending around 12th week

Mid gestation –> inguinal canal

End –> scrotum (in 12 last weeks)

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4
Q

2 major histological components of the testicles:

A
  1. Leydig/C cells (interstitial)
  2. Seminiferous tubules
    1. Germinal cells
    2. Sertoli cells
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5
Q

Hormones in Leydig cells:

A
  1. 95% testosterone
  2. DHT
  3. Estradiol

Small amounts of: dehydroepiandrosterone, androstenedione

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6
Q

What do Sertoli cells secrete?

A

Anti-Mullerian hormone (HAM)

Androgen binding protein

Inhibine

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7
Q

Function of seminiferous tubules:

A

Production of spermatozoids –> NO HORMONE PRODUCTION

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8
Q

Where else can androgens come from?

A

Andrenal glands:

  • DHEA
  • DHEAS
  • Androstenedione –> testosterone (peripheral)

Precursor conversion:

  • Estradiol, estrone
  • DHT
  • Testosterone
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9
Q

How is testosterone transported throughout the body?

A

Bound to proteins:

  • SHBG (44%)
  • Albumin (52%)

Free (2%) –> active testosterone

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10
Q

Mechanism of action of androgens:

A

Testicles –> testosterone

Partially converted into DHT by 5-alpha-reductase

DHT and testosterone have the same receptor BUT different function

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11
Q

What are the roles of testosterone?

A
  1. Regulation of FSH and LH
  2. Initiation and maintenance of spermatogenesis
  3. Formation of “male phenotype” –> voice, muscles, virilization
  4. Sexual maturation during puberty
  5. Control of libido
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12
Q

What are the roles of testosterone during embryogenesis?

A

Direct role: differentiation of male internal genital organs

Indirect role: differentiation of male OGE

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13
Q

What are the roles of testosterone during puberty and in adults?

A

Puberty: secondary sexual characteristics

Adult: libido/potency

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14
Q

Axe hypothalamo-hypophyso gonadique

A
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15
Q

Three sequential processes of sexual differenciation:

A
  1. Chromosomes: XX vs XY
  2. Gonadal sex: undifferentiated –> ovary vs testicle
  3. Somatic sex: development of external genitalia
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16
Q

Steps of somatic sex determination:

A
  1. 8-10 weeks: regression of muller canals (HAM secretion by Sertoli)
  2. 9 weeks: differentiation of Wolff canals (testosterone by Leydig)
  3. 10 weeks: OGE
  4. Testicular descent:
    • 12 weeks: abdomen –> inguinal canal
    • 7 months: inguinal canal –> scrotum
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17
Q

Testicular differentiation:

A
  1. Sertoli cells –> HAM
    • Regression of Muller canals
  2. C Leydig cells
    • Start synthesis of testosterone:
      1. Differentiation of Wolff canals
      2. Spermatogenesis
      3. External virilisation (DHT (5 alpha-reductase))
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18
Q

Embryological biosynthesis and regulation of testosterone:

A

First and second trimesters:

  • HCG (placenta) –> stimulus that maintain testicular steroidogenesis
  • FSH and LH have NO ROLE

Third trimester:

  • Axe hypothalamo-hypophysaire gonadique starts working
  • FSH –> stimulates the growth of seminiferous tubules
  • LH –> stimulates the production of testosterone in Leydig cells
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19
Q

What is dihydrotestosterone (DHT)?

A

Shares the same receptor as testosterone

Stronger than testosterone (higher affinity and stability)

Masculinisation of OGE (penis, scrotum, and prostate)

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20
Q

Action of testosterone in utero:

A

Masculinisation of fetus (XY presentation)

Differentiation of Wolff canals –> epididymis, vas deferens, seminal vesicles, ejaculatory canal

NO DIRECT ACTION OF DIFFERENTIATION OF UROGENITAL SINUS

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21
Q

What is 5 alpha-reductase?

A

The enzyme necessary for the conversion of testosterone –> DHT

Present in:

  • Prostate
  • Urogenital sinus
  • OGE

Not really present in:

  • Wolff canals
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22
Q

How does testosterone vary with age?

A

Birth: mini puberty around 6 weeks

Puberty: progressive increase of testosterone secretion

Adult: stable max levels

Elderly: gradual decrease of testosterone secretion

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23
Q

Frequent causes of sexual differentiation problems

A
  1. Congenital adrenal hyperplasia
  2. Anomalies with testosterone synthesis/action
  3. Androgen insensibility
  4. Deficit in 5 alpha-reductase
  5. Anomalies of cholesterol synthesis
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24
Q

What is puberty?

A

Ensemble des phénomènes physiques, psychiques, mentaux, affectifs qui caractérisent le passage de l’enfance –> adulte

Takes around 4 years

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25
Q

Physiology of puberty:

A

Axe hypothalamo-hypophyso-gonadique inactive during prepubescence

GnRH –> reamplification of its pulsatility

​​Pituitary:

  • increased sensitivity to GnRH and LH/FSH (LH>FSH)
  • Gonadic maturation –> secondary sexual characteristics
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26
Q

What factors influence the start of puberty?

A
  • Genetics
  • Age of puberty in parents
  • Bone age
  • Integrity of the axe
  • Growth hormone
    • Facilitates the start of puberty
  • Nutrition
  • Fatty tissue
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27
Q

What characterizes puberty in boys?

A
  1. Apparition of secondary sexual characteristics
  2. Growth spurt
  3. Peak of bone density
  4. Increased muscle mass
  5. Gynecomastia (50-60%)
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28
Q

What is an orchidometer?

A

medical instrument used to measure the volume of the testicles

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29
Q

Tanner stages of male puberty:

A
30
Q

Chronology of puberty in boys:

A
  1. Increased testicular volume (1st sign of puberty… has to be > 4 cm)
  2. Pubic hair
  3. Penis growth
  4. Growth spurt
  5. Axillary hair growth (12-18 months later)
  6. Voice drop (12 months later)
  7. Facial hair (Tanner 4/5)
31
Q

What is gynecomastia?

A

Benign proliferation of glandular tissue IN MEN

Presence of firm, concentric mass under areola

32
Q

What is adipomastia?

A

Accumulation of fat without glandular proliferation

33
Q

Physiopathology of gynecomastia:

A
34
Q

Physiological causes of gynecomastia:

A

Newborn, puberty, old age

35
Q

Gynecomastia in newborns:

A

In 60-90% of newborns

Transitory –> disappears in 2-3 weeks

Maternal passage of milk

Galactorrhea

36
Q

Gynecomastia during adolescence:

A

Transitory increase in mammary tissue in 50-60% of teenage boys

Usually happens around age 14 and disappears after around 18 months

No galactorrhea

Rare to still be present after 17 years old

37
Q

What is macromastia?

A

Severe gynecomastia (> 4cm)

Can persist pas adolescence

Often associated with an endocrinopathy

38
Q

Physiopathology of gynecomastia in adolescents:

A

Relative increase in estradiol compared to testosterone

Increased estrone compared to other adrenal androgens

Local formation of estradiol in mammary tissue

39
Q

Age linked gynecomastia

A

In 24-65% of men between the ages of 50-80 years old due to a decrease in testosterone production

40
Q

Pathological causes of gynecomastia:

A

Relative excess of estrogen/relative decrease of testosterone:

  1. Klinefelter Syndrome (47 XXY)
  2. Congenital anorchia
  3. Androgen insensitivity (46 XY but presents as XX)
  4. Secondary testicular insufficiency

Increase In estrogen production:

  1. Testicular tumours, hermaphroditism, hCG secreting tumours
  2. Increased substrate for aromatase (converts testo –> estro)
    1. Adrenal/hepatic insufficiency, hyperT4
    2. Increased extraglandular aromatase
41
Q

Other pathological causes of gynecomastia:

A

Medication, drugs, idiopathic (no known cause even after tests)

42
Q

Bilan for gynecomastia:

A

FSH/LH

Estradiol and testosterone

TSH and T4

Karyotyping (47 XXY?…)

Spermogram

bHCG, alpha foeto-protein

AST, ALT, BUN, Creat.

43
Q

What is hypogonadism?

A

Decrease in at least 1/2 functions of the testicles:

  1. Spermatogenesis
  2. Testosterone production

Can be caused by:

  1. Testicular issue –> primary
  2. Hypothalamus/pituitary –> central
44
Q

Hypogonadism in adolescents:

A

Absence or stop of puberty

Gynecomastia/anosmia

Decreased growth speed except for in Klinefelter

Loss of bone density

45
Q

Hypogonadism in adults:

A

Infertility and loss of libido

Gynecomastia

Osteoporosis

46
Q

Complications of hypogonadism:

A

Infertility

Osteoporosis

Gynecomastia

Psychological repercussions

47
Q

Central hypogonadism: decrease/loss of secretion of LH and FSH

A

Associated with:

  • Dim. spermatogenesis
  • Dim. testosterone
  • Possible cryptorchidism depending on when it started
  • Small testes

Not typically associated with gynecomastia (FSH and LH not increased therefore less aromatase stimulation)

48
Q

Central hypogonadism: congenital

A

Causes:

  1. Kallmann Syndrome
  2. SNC malformation
  3. Isolated –> GnRH-R mutations, LH-B or FSH-B butations
  4. Syndrome associated: Bradet-Biedl/Prader-Willi
  5. Idiopathic
49
Q

Central hypogonadism: acquired

A

Any damage to hypothalamus/pituitary:

  • Tumors –> craniopharyngioma/histyocysosis
  • Trauma
  • Infections
  • Gonadal steroids (Rx)
  • Chronic illnesses
  • Anorexia
50
Q

Central hypogonadism: endocrine

A
  1. Cushing
  2. HypoT4
  3. Hypopituitarism
  4. HyperPRL (interferes with FSH/LH secretion)
51
Q

What is Kallmann Syndrome?

A

Anomaly with the migration/adhesion of GnRH neurons (with smell) –> anosmia

Transmission: autosomal dominant, recessive, X-linked, sporadic, familial

Associated with:

  • Anosmia/hyposmia
  • Median line anomalies
  • Neurosensorial deafness
  • Colour blindness
52
Q

How to dx central hypogonadism?

A

Labs:

  • Dim. testosterone
  • Dim. LH/FSH
  • Dim. spermogram

Imagery:

  • Lowered bone density
  • Bone age
  • MRI
53
Q

What is primary hypogonadism?

A

Testicular problem

Usually more serious impact on spermatogenisis

  • Low/normal testosterone
  • Increased +++ FSH/LH
54
Q

Most common causes of primary hypogonadism:

A
  • Chromosomal: Klinefelter
  • Chimio/radiotx
  • Infectious: orchite/oreillons
  • Testicular torsion/trauma
  • Congenital anorchia
  • FSH-R/LH-R mutations
  • Mutations with steroidogenesis enzymes
55
Q

What is Klinefelter Syndrome?

A

47 XXY (usually due to egg being XX but can be due to XY sperm in rare cases)

1/500-1/1000 births

More frequent if mother is older

Expression during puberty/adult age… not possible to know at birth without checking for it

56
Q

Presentation of Klinefelter

A

Before puberty: NO SIGNS, but can have behaviour/school issues

Puberty:

  • Stagnation of puberty
  • Small testicles
  • Eunoichidism
  • Gynecomastia
  • Tall, long arm/legs
  • Degeneration of seminiferous tubules (fibrosis) –> testicular shrinkage and can lead to azoospermia
  • Increased estradiol –> increased SHBG
  • Dim. testosterone

Adulthood:

  • Small testicles/eunochoidism
  • Gynecomastia
  • Decreased hair
  • Infertility
  • Osteoporosis
57
Q

Diagnosis of Klinefelter

A

Clinical presentation

Biologic: dim. testo, increased LH/FSH

Karyotyping (47 XXY)

58
Q

Prevalence of testicular tumours

A

1-2% of malignant tumours in men

4-10% of genitourinary cancers

2nd most common cause of cancer in men between 20-34 years old

59
Q

Causes of testicular tumours

A

Cause is really unknown

FDR:

  • Cryptorchidism
  • Testicular dysgenesis
  • Trauma?

Bilat. gynecomastia quite rare

60
Q

What are the two kinds of testicular tumours?

A
  1. Germinal cell tumours
  2. Leydig tumours
61
Q

Germinal cell tumours

A

Seminomas –> 33-50%

Tumeurs des C embryonnaires –> 20-33%

Teratomas –> 10-30%

Choriocarcinomas –> 2%

Tumoural markers:

  • bHCG +++
  • afoeto-protein
62
Q

Clinical presentation of germinal cell tumours

A

Increased testicular volume (no pain)

“Sensation de plénitude”

80% –> tender mass

25% –> pain/increased sensitivity

6-25% –> history of trauma

5-10% –> Sx of metastasis

Can cause premature puberty

63
Q

Leydig cell tumours

A

Children: premature puberty (increased speed of growth, bone density, development of secondary sexual characteristics)

Teens: accelerated growth, testicular masses

Adult: unilateral testicular mass, gynecomastia, if tumour Is active (endocrine)

  • Decreased FSH and LH –> decreased testosterone
  • Loss of libido
  • Azoospermia
64
Q

What is andropause?

A

Progressive loss of gonadal function with age (usually after 50 years old)

65
Q

Physiology of andropause:

A

A gradual decrease of testosterone secretion with an increase in SHBG

Decreased response in Leydig cells to hCG

Increase in LH (compensation)

Histopathology: degeneration of seminiferous tubules and # and volume of Leydig cells

Also due to microvascular insuff.

66
Q

Clinical presentation of andropause

A

Loss of libido

Erectile dysfunction

Emitonal instability

Fatigue/loss of concentration

Loss of muscle mass/force

Vasomotor instability (palpitations, hot flashes, diaphoresis)

Diffuse myalgia

IF SEVERE –> loss of testicular volume/texture

67
Q

Lab findings in andropause

A

Low/low normal testosterone

LH in limits of normal or slightly high

Spermogram: oligospermia

Loss of bone density (dim. minérilisation osseuse)

68
Q

What are the indications for taking testosterone?

A

Induce and maintain puberty –> kids and teens

Hypogonadism –> adults

69
Q

Goals of testosterone replacement therapy

A

Induce/restore:

  • Secondary sex characteristics
  • “Male” behaviour

Assure proper somatic development

70
Q

Side effects of taking testosterone:

A

Intrahepatic cholestasis

Hepatocellular carcinoma

Premature epiphysis closing (in kids)

Hydrosodium retention

Erythrocytosis

Gynecomastia

Priapism, acne, aggressiveness

Oligospermia and testicular atrophy

71
Q

How is testosterone administered?

A

IM injections

S/C injections

Transdermal gel

Transdermal patch (scrotal, non scrotal, gel)

ORAL IS NOT YET AVAILABLE

MD1 endocrinologie (6 decks)

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