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Endocrine > Childhood growth / puberty > Flashcards

Childhood growth / puberty Flashcards

1
Q

Speed / control of intrauterine growth

A

Very fast

IGF1 / 2, insulin

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2
Q

Speed / control of early infancy growth

A

Rapid, but declining
Controlled by nutrition (insulin, IGF)
Get post-natal “mini puberty”

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3
Q

Speed / control of childhood growth

A

Gradually slows until puberty

Controlled by GH. TH necessary for GH secretion.

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4
Q

Speed / control of pubertal growth

A

Rapid growth until fusion of epiphyseal plates.
Androgens stimulate growth plate.
Estrogens stimulate GH secretion and growth plate closure.

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5
Q

GH effects on adipose tissue (5)

A

Increased lipolysis, stimulated hormone sensitive lipase, inhibited lipoprotein lipase, decreased glucose transport, decreased lipogenesis

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6
Q

Genetics of CDGP

A

Autosomal dominant. Often strong family history.

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7
Q

3 general causes of non-familial intrinsic short nature

A

Genetic / chromosomal problems: Turner, Russel-Silver syndromes
Prenatal: IUGR
Postnatal: spinal radiation

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8
Q

Endocrine vs disease-causing attenuated growth

A
  • Endocrine problem – stature is affected more than weight. Ex: Hypothyroid, low GH, or glucocorticoid excess
  • If both height and weight are increasing percentiles, it is NOT an endocrine cause.

•Underlying disease – weight affected more than stature. Often a calorie problem. Ex: renal disease, IBD.

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9
Q

What happens if GH is low in utero?

A

No lack of growth, but hypoglycemia may occur

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10
Q

2 physical effects of low GH (not height-related)

A
  • Males may exhibit lack of phallic growth b/w 6-12 months of age.
  • Faces are typically fair and “cherubic” and may manifest in midline defects such as hypotelorism, cleft palate, poor nasal bridge development, or single central incisor.
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11
Q

Which diseases is GH FDA-approved for? (4)

A

GH deficiency, familial short stature, IUGR, Turner syndrome

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12
Q

What is the most common cause of accelerated growth?

A

Over-nutrition. Weight usually affected more than height.

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13
Q

What is adult height if CAH or precocious puberty is not treated?

A

Short due to premature closure of epiphyseal growth plates.

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14
Q

When does adrenarche usually occur?

A

Age 6-8

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15
Q

When does telarche usually occur?

A

Age 10

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16
Q

What determines testicular size?

A

FSH / LH

Not testosterone

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17
Q

Avg age of menarche

A

Age 12.5

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18
Q

What does Kisspeptin do?

A

Releases blockage on GnRH –> increased GH, IGF1, FSH, LH, estrogen, and testosterone.
Pituitary also becomes more sensitive to GnRH.

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19
Q

Tanner breast stage II

A

Breast budding

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20
Q

Tanner breast stage III

A

Glandular tissue develops

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21
Q

Tanner breast stage IV

A

Areola and papilla form secondary mound

22
Q

Tanner breast stage V

A

Mature breast

23
Q

What tanner stage are most kids at at start of puberty?

A

Stage III

24
Q

Tanner hair stage II

A

Sparse, pigmented, long, straight hair mainly along labia and base of penis

25
Q

Tanner hair stage III

A

Darker, courser, curlier

26
Q

Tanner hair stage IV

A

Adult hair, but not full distribution yet

27
Q

Tanner hair stage V

A

Adult hair w/ spread to medial thighs

28
Q

Tanner hair stage VI

A

Midline hair up abdomen. Abnormal in females.

29
Q

Ages of precocious puberty
White / AA girls
Boys

A
  • Under 8 Caucasian girls
  • Under 7 African American girls
  • Under 9 boys
30
Q 
Central precocious puberty
Male causes
Female causes
Associations
Treatment
A
  • Males – CNS causes are predominant, such as tumors, injury, or other sex steroids.
  • Females – often idiopathic. Many are caused by hypothalamic hamartomas.
  • Associated w/ hydrocephalus, closed head injuries, and cerebral palsy
  • Treat w/ long-acting GnRH analogs
31
Q

3 gonadal causes of peripheral precocious puberty

A

Sex hormone-secreting gonadal tumors
McCune-Albright Syndrome
Familial testotoxicosis

32
Q

McCune-Albright Syndrome
Cause
Sxs (3)

A
  • Etiology - G protein defect in gonadotropin receptor.

* Sxs - Kids have café-au-lait spots, polyostotic fibrous dysplasia, and rapid growth.

33
Q 
Familial testotoxicosis
Etiology
Inheritance
Sxs
Prognosis
A
  • Etiology - Testes contain a constitutively activated LH receptor.
  • Inheritance - Transmitted from father to son.
  • Sxs - Toddlers present w/ penile enlargement, pubic hair, and behavior problems.
  • Prognosis - Without treatment, these boys are below 3rd percentile for height due to rapid bone age advancement.
34
Q

2 adrenal causes of precocious puberty

Treatment

A

CAH and virilizing adrenal tumors

Treat w/ glucocorticoids to lower ACTH

35
Q

Ages of delayed puberty
Breast
Menses
Boys

A

> 14 years (breast)
16 years (menses)
15 years in boys

36
Q

Most common cause of delayed puberty in US vs worldwide

A

US: constitutional growth delay
World: malnutrition

37
Q

Causes of secondary hypogonadotropic hypogonadism (7)

A

Anorexia, athlete triad, male obesity (fat tissue has aromatase activity, converting testosterone to estrogen), chronic disease, malnutrition, endocrine disease (HYPOTHYROID, HYPERPROLACTINEMIA), celiac disease.

38
Q

Athlete triad

A

Disordered eating, amenorrhea, osteoporosis

39
Q

Causes of hypergonadotropic hypogonadism

A
  • Intrinsic gonadal dysgenesis – Turner and Klinefelter are 2 most common
  • Gonadal damage – chemo, radiation, galactosemia
  • Others – trauma, autoimmune, inflammation / infection, infiltration
40
Q

Characteristics of Klinefelter

A

Tall stature, gynecomastia, visceral adiposity

41
Q

Treating delayed puberty in girls vs boys

A
  • Girls – increasing doses of estradiol over 9-12 months to promote normal puberty w/o rapidly advancing bone age. Progesterone is added after 9-12 months to induce menses cyclically.
  • Boys – monthly testosterone therapy in increasing doses.
42
Q

Premature thelarche / adrenarche

Population

A
  • This is a normal variation. Do NOT remove breast tissue b/c it will not grow back later.
  • Premature thelarche usually occurs in 1-3 y/o girl without any other signs of puberty.
  • Premature adrenarche is more common in AA’s and obese children.
43
Q

Characteristics of isolated pubertal changes

A
  • Not true CNS puberty. Premature thelarche / adrenarche may occur.
  • No gonadotropin activation
  • Minimal / no growth or bone age acceleration
  • Increased risk for metabolic syndrome and PCOS.
  • Normal age of onset of true puberty
44
Q

Constitutional growth delay
Growth velocity
What drug do they qualify for?

A
  • Normal growth velocity.
  • Do NOT qualify for GH.
  • Oxandrolone is weak male hormone that does NOT get converted to estrogen (closes growth plate). Promotes growth and weight. Catches kids up to peers, but doesn’t make them taller than they would have been w/o it.
45
Q

Familial short stature

Do they cross percentiles?

A

Cross percentiles downward in first 3 years after nutrition –> GH / genetics phase.

46
Q 
Non-familial genetic short stature
Cross percentiles?
Bone age
#1 cause
Other cause
Treatment
A 
Yes cross percentiles
Bone age = chronological age
#1 cause is Turner syndrome
Other cause is IUGR
GH is approved
47
Q

Characteristics of Turner Syndrome (7)

A
  • Ovarian insufficiency → no estrogen → no puberty
  • Edema of hands due to congenital problems of lymphatic drainage
  • Ear infections: facial features are downturned, possibly leading to increased predisposition to infection
  • Webbed neck also due to anomaly in lymphatic drainage
  • Wide carrying angle
  • Coarctation of the aorta
  • Renal problems may involve horseshoe kidney and double ureters (increased risk of UTI)
48
Q 
Endocrine-related attenuated growth
Cross percentiles?
Bone age
Adult height
Does birth weight play a role?
A

Yes cross percentiles
Bone age less than chronological age
Adult height is less than mid-parental height
Birth weight does NOT play a role

49
Q

4 clues for GH deficiency

A
  • Microphallus (due to low FSH / LH)
  • High arched palate
  • Subcutaneous fat
  • May present w/ hypoglycemia due to lack of counter-regulatory hormones (ACTH, GH)
50
Q

GH effects on muscle / fat

A

GH plays a role in increasing lean body mass and decreasing fat. Low GH → short fat baby

51
Q

Genetics of Kallman syndrome

A

May be autosomal dominant (FGFR1 gene), recessive, or X linked (KAL1 gene)

Endocrine (24 decks)

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