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PNP: Physical Assessment - BK > Growth > Flashcards

Growth Flashcards

1
Q

Vital Sign Tips

A

Respiratory rate and heart rate should be counted for a full minute with child calm and at rest

Each degree of Fahrenheit increases the HR 8-10 beats/ minute

Blood pressure When you have difficulty getting a blood pressure from a patient (i.e., it is too “quiet” to hear it), have the patient raise up their arm to help make it louder Sex, age, weight

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2
Q

Pubertal Growth Spurt

A

Girls = 8-12cm (3-5in) Boys = 10-14 cm (4-6in)

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3
Q

Why are measurements so important?

A

Clinical decisions and clinical interventions are based on physical measurements Accurate and reliable physical measures are used to: - Monitor the growth of an individual - Detect growth abnormalities - Monitor nutritional status - Track the effects of medical or nutritional intervention **IF YOU DO NOT FEEL COMFORTABLE WITH A MEASUREMENT YOU NEED TO REPEAT IT!**

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4
Q

Growth Charts – weight for age

A

Reflects body weight relative to age Influenced by recent changes in health or nutritional status. Not used to classify infants, children and adolescents as under or overweight. Used in early infancy for monitoring weight and helping explain changes in weight-for-length and BMI-for-age in older children.

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5
Q

Stature/Length-for-age

A

Linear growth relative to age Used to define shortness or tallness

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6
Q

BMI for age

A

Anthropometric index of weight and height Used to classify children and adolescents as underweight, overweight, or obese.

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7
Q

Weight for length/stature Head circumference

A

Weight-for-length/stature reflects body weight relative to length and requires no knowledge of age. Indicator to classify infants and young children as overweight and underweight Head circumference-for-age is critical during infancy and can be charted up to 36 months of age. Measurements reflect brain size.

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8
Q

Head circumference positioning

A

Proper positioning of measuring tape Widest circumference, avoiding ears

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9
Q

BMI for age

A

>95th percentile – Obese

>85th and <95th percentile = overweight

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10
Q

Weight for length/stature

A

>95th percentile – Obese

<5th percentile = underweight

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11
Q

Stature/length for age

A

<5th = short stature

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12
Q

Head circumference for age

A

95th percentile = developmental problems

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13
Q

BMI

A

Body fatness changes as children grow Girls and boys differ as they mature BMI declines and reaches a minimum around 4-6 years of age before beginning a gradual increase through adolescence and most of adulthood

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14
Q

BMI is a Screener

A

BMI is not a direct measure of body fatness.

However, BMI parallels changes obtained by direct measures of body fat such as underwater weighing and dual energy x-ray absorptiometry (DXA).

BMI can be considered a proxy for measures of body fat. BMI will change with age so it must be plotted

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15
Q

SGA

A

A birth weight and/or length greater than 2 SD below the mean It is below the 10th percentile in weight, length, or HC

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16
Q

LGA

A

babies are those babies who are greater than 2SD above the mean Birth weight (or length, or HC) lies above the 90th percentile for that gestational age

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17
Q

STATURAL growth

A

A complex process that is determined by the interaction of Genetics Nutrition Socioeconomic factors

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18
Q

Abnormally Rapid Growth Velocity Midparental height

A

Determining heights of biological parents is of critical importance

Girls: Father’s height + Mother’s height - 5 in.//2

Boys: Father’s height + Mother’s height +5 // 2

Target height = midparental height = 2SD

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19
Q

Physical exam for growth

A

Dysmorphic features

Midline defects

Skin

Neck

Sexual exam

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20
Q

Deciphering Problematic Growth Curves

A

Is the growth rate normal or abnormal? Look at as many points as possible Is there abnormal tempo of growth? Bone age Are there underlying reasons for intrinsic/genetic short stature? History, mid parental height, PE findings Do the answers to these questions fully explain child’s position on the growth curve? Convergence of multiple growth patterns in one child

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21
Q

Confounding Factors - Obesity

A

Obese children are taller With endocrinopathies, height is impaired If the child’s ht. is at or greater than mid parental height, an endocrine cause of the obesity is unlikely

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22
Q

Genetic Channeling

A

Upward to downward movement toward mid parental range Usually accomplished by 12-15 months

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23
Q

Constitutional growth delay - Risk Factors

A
  • Family history
  • The child is healthy, growing below but parallel to the 3rd percentile line
  • Between 6-24 months, the linear growth and weight track downward to the 3rd percentile
  • Slow growth rate between 12-30 months
  • Delayed onset of puberty and a growth spurt and usually end up with heights in the lower half of the normal range.
  • Bone age that is delayed by 2 or more years
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24
Q

Confounding Factors in Late Childhood Growth

A

Infrequent measurement opportunities Normal prepubertal growth deceleration Effects of medications for common disorder (ADHD, asthma, depression) Normal variation in onset of puberty

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25
Q

Key information required to decipher a child’s growth curve

A

Birth length and weight (SGA vs. prematurity)

Mid parental height

Family growth and pubertal history

Growth rate-normal for age

Bone age (Left wrist)-contributions of delayed vs genetic/intrinsic growth disturbance

Health history – effects of disease on growth

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26
Q

Bone age

A

Bone age is a measure of skeletal maturity.

A conventional X-ray of the left hand and wrist to evaluate bone age may be obtained at the initial visit to assess skeletal maturation, and may be repeated over time if needed

The methods used most commonly for determining bone age are the Greulich and Pyle Atlas and the Tanner- Whitehouse (TW2) method

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27
Q

Skeletal Maturation

A

Occurs under the influence of estrogen, thyroid hormone, androgen and growth hormones Bone are is generally more than 2 years in advance of chronologic age in long-standing precocious puberty because of the action of sex hormones

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28
Q

General screening tests in the evaluation of abnormal growth in children (7)

A

CBC – anemia, blood dyscrasia, infections

BMP – rules out renal disease and electrolyte abnormalities that could occur with Barter syndrome, other renal or metabolic disorders and diabetes insipidus

Liver functioning testing Assesses metabolic or infectious disorders associated with liver dysfunction

Urinalysis and urine pH level Assesses kidney function and rules out renal tubular acidosis

Erythrocyte sedimentation rate Evaluates for chronic inflammatory states

GH deficiency IGF-1, IGF binding protein 3 Hypothyroidism – free thyroxine, TSH

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29
Q

Sexual Maturity Rating (SMR; Tanner staging)

A

Males

Size of the testes

Length of the penis

Hair development

Females Breast development Public hair development

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30
Q

Body Fat

A

Body fat continually increases in girls during most of the second decade, while boys tend to decrease fat after age 14. In the lower ranges, BMI-for-age tends to increase more slowly in both adolescent boys and girls. At the 5th percentile, BMI-for-age increases at the rate of about 0.5 unit/year during most of the second decade.

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31
Q

Female Puberty

What is first and what percentage

A

The appearance of breast buds in girls are the earliest signs of pubertal development in 85%

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32
Q

Puberty and Females (3)

A

Sexual maturity rating (tanner stage) Breast budding (Thelarche is the first sign in 85%) Public hair growth (Pubarche) is the initial pubertal sign in 15% of girls

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33
Q

Menarche occurs an average of ________ after thelarche

A

2 years Range is 1 to 5 years

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34
Q

Peak height velocity reached

A

at 12 years in girls immediately prior to menarche

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35
Q

Early in puberty

A

Slow their accumulation of total body fat, but during their peak height velocity they accelerate their accumulation of fat and lean body tissue, leading to an increase in weight that peaks just prior to menarche.

After that time, the rate at which weight is added slows, with an inflection point around 13 years of age.

Between the age of 12 and 13, girls at the 5th percentile gain less than 8 lbs. while those at the 95th percentile gain more than 13 lbs.

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36
Q

TANNER STAGES BREAST

A

Tanner 1 = none

Tanner 2 = breast bud diameter = areola width

Tanner 3 = Breast diameter >areolar width

Tanner 4 = Mounding of areola above plane of breast

Tanner 5 = Adult

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37
Q

TANNER FEMALE PUBIC HAIR

A

Tanner 1 = none Tanner 2 = slightly pigmented over mons or labia Tanner 3 = dark, coarse, on mons Tanner 4 = Adult in character, confined to mons Tanner 5 = Adult spread to medial thigh

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38
Q

Male Puberty

Testicular volume and prepubescent and pubescent boys

A

In boys, testicular size should be measured by a Prader orchidometer.

A testicular volume of > 4 mL in boys indicates puberty is starting

Prepubescent boys testicle equals 2.5 cm in length

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39
Q

Male puberty

Increase in stature due to _______

PHV?

A

The increase in stature in males is due to androgens produced by the testes, so the growth spurt in stature is preceded by an increase in the size of the testes.

Androgens also cause the penis to lengthen and widen

Pubertal development is slow to SMR stage III

Accelerate with a total four years between stage II and V PHV is achieved at age l4 years

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40
Q

TANNER GENITALIA MALE

A

Tanner 1 = Prepubertal testis <2cm

Tanner 2 = prepubertal testis 2.5 cm, volume 4mL

Tanner 3 = Phallus has grown in length; testes >3cm, volume 6mL, 8mL

Tanner 4 = Phallus has grown in breath; testes > 4cm Volume 10mL/15mL

Tanner 5 = adult testes >5cm; volume >15mL

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41
Q

Male Tanner again

A

GENITAL DEVELOPMENT (MALE)

  • Stage Preadolescent
    • Testes, scrotum, and penis about same size and proportion as in early childhood
  • Enlargement of scrotum and testes
    • Skin of scrotum reddens and changes in texture; little or no enlargement of penis
  • Enlargement of penis
    • First mainly in length; further growth of testes and scrotum (11.5-14
  • Increased size of penis with growth in breadth and development of glans
    • Further enlargement of testes and scrotum and increased darkening of scrotal skin (13.5-15)
  • Genitalia adult in size and shape
42
Q

Adolescence and Alkaline Phosphatase

A
  • With rapid bone growth, alkaline phosphatase levels increase
  • Level can be 50-100% above the normal range.
  • Peaks at about the peak height velocity in males and females so occurs earlier in females
43
Q

Delayed Puberty Definition

A

Delayed puberty is defined clinically by the absence or incomplete development of 2nd sexual characteristics by an age at which 95 % of children of that sex and culture have initiated sexual maturation.

44
Q

Delayed puberty ages for upper 95%

A

The upper 95th % in the U.S. for age is: boys 14 years of age girls 12 years of age

45
Q

Definition of Precocious puberty GIRLS (8)

A

Breast development

Precocious puberty

  • Any sign of puberty in girl less than 8
  • Boys less than 9
  • Within creases to tanner 3 within a 6-12 month period in a 6-8 year old
  • Wait in a girl with 2cm or less of glandular tissue and no increase in growth
  • Menarche before age 10 years
  • Pubic Hair White: Before age 7 years Black: Before age 6 years
46
Q

Adrenarche (5)

A
  • Increased adrenal androgen secretion
  • Occurs between ages 6 to 8 years
  • Transient growth spurt
  • Some children develop axillary and pubic
  • No sexual development occurs
47
Q

Gonadarche: GnRH released Boys vs. Girls

A

Boys

LH stimulates Testosterone production

FSH stimulates sperm maturation

Girls

FSH stimulates

Estrogen and follicle formation LH stimulates corpus luteum after Ovulation

48
Q

Mean age of Menarche

A

African America = 12.2 year Caucasian = 12.9 year Boys = precocious puberty less than 9 years

49
Q

Hypergonadotropic hypogonadism vs. Hypogonadotrophic hypogonadism

A

There are two major categories: Hypergonadotropic hypogonadism (high luteinizing hormone [LH] and follicle-stimulating hormone [FSH]) is secondary to primary gonadal failure. Hypogonadotropic hypogonadism (low or normal LH and FSH) is secondary to constitutional delay or a central gonadotropin deficiency.

50
Q

Precocious Puberty

A

Any sign of secondary sexual maturation before 8 years in girls and 9 years in boys. More recent data suggests early puberty may not warrant extensive evaluation or intervention if it occurs after 6 years in African-American girls or after 7 years in Caucasian girls (Herman- Giddens, 1997).

51
Q

Red flags for pathologic pubertal development

A
  • Contrasexual development
  • Feminization in boys—gynecomastia
  • Virilization in girls – Clitoris enlargement, acne Peripheral cause (often asynchronous development)
  • Penis enlarges without scrotal enlargement
  • Extensive pubic Hair Growth
  • Menarche without breast bud development in girls
  • Precocious Puberty in boys (50% pathologic)
  • Rapid growth in breast development through tanner III in an 8 year old or less
  • Enlargement of the penis without enlargement of the testicle
  • Documented growth acceleration in a child over 6-12 months in a girl less than 8 or a boy less than 9
  • Any virilization signs such as clitoris enlargement, voice deepening or increase in muscle mass.
52
Q

Precocious Puberty TYPES

A
  • Incomplete precocious puberty:
    • Premature thelarche
    • Premature adrenarche
  • GnRH and gonadotropin independent puberty
    • FSH and LH suppressed
  • True and complete (central precocious Puberty)
  • Pseudoisosexual Puberty
53
Q

Pseudo-precocious puberty

A

Some of the changes of puberty are present But appearance is isolated or out of normal sequence

54
Q

Isosexual puberty

A

When the changes of puberty are consistent with child’s gender

When they are discordant with gender, they are heterosexual

55
Q

True precocious puberty

A

Early pubertal changes

Normal progression in order of breasts, pubic hair development, growth spurt

For females, menstruation

56
Q

Premature thelarche

A
  • Development of breast buds
  • Most common variation
  • Usually 1-4 years of age
  • Usually benign if not associated with onset of other pubertal events
57
Q

Precocious puberty should be suspected if

A
  • Breast, nipple and areolar development reach tanner 3
  • Linear growth accelerates
  • Androgenization with pubic and/or axillary hair
58
Q

Premature thelarche or precocious puberty

A

Premature thelarche 6mo-2yr

Breasts: Usually II, early III regresses in 80%

no pubic hair, axillary hair, apocrine odor, menses, accelerated growth, advanced bone age, considered benign

Precocious puberty 5-8 years

Breasts: II through V; does not fluctuate in size Public hair or axillary hair+breast

YES apocrine odor, menses, accelerated growth, advanced bone age, early puberty = SHORT STATURE

59
Q

NORMAL VALUES

FSH LH Estradiol Bone age

A

0-2.8

0-1.6

<25 - estradiol

Bone age – with age

60
Q

Premature Adrenarche + Physical Assessment

A
  • The growth of axillary hair stimulated by androgen
  • Look for androgen exposure
  • Family history (partial forms of adrenal hyperplasia)
  • Look at breasts for female
  • Testicular enlargement for male
  • Axillary hair is only finding, check in 3-4 months
  • Acne
  • Enlargement of the clitoris
61
Q

Clinical Eval of Precocious Puberty

A

Pubertal signs

Age of onset

Rate of progression

Growth pattern

62
Q

Clinical Evaluation of Precocious Puberty: History

A

Past medical history

  • CNS insults
  • Exposure to environmental sex hormones
  • Serious illnesses
  • Any symptoms

Check regarding family history of sexual precocious

Sibling with ambiguous genitalia

Family may consider precocious puberty normal

63
Q

Clinical Eval of Precocious puberty (4) clinical aspects

A

Plot height, wt., and head circumference (if less than 3 years) Will be rapid if CPP or pseudoisosexual precocious puberty

Height will rise to higher growth percentile than occupied previously

Blood pressure hypertension may suggest Congenital adrenal hyperplasia due to deficiency of 11 beta hydroxylase)

Sexual maturity Are there breast buds? Have they regressed from birth? Is this a new process?

Signs of systemic disease

64
Q

Clinical Eval of PP

Look for evidence of CNS mass

Evidence of androgenic influence

Evidence of any other mass

A

MASS: Optic fundus; Visual fields

  • Acne Facial and axillary hair
  • Increased muscle bulk
  • Extent of pubic hair
  • Penile elongation
  • Scrotal rugation increased with thinning
  • Clitoris enlargement

Asymmetric testicular enlargement

Hepatomegaly Abdominal mass

65
Q

5 Clinical evals for PP

A

Cafe au lait spots

Myxedematous face

Thyroid enlargement

Abnormal visual field

Abnormal neuro findings

(hyperreflexia = brain tumor = UMN disease; hyporeflexia = LMN disease

66
Q

Evidence of estrogenic influence Evidence of gonadotropic stimulation Pseudoisosexual precocious puberty

A

Evidence of estrogenic influence

  • Size of breast tissue
  • Must distinguish breast from soft smooth consistency of increased fat
  • Reddish, less moist vaginal mucosa in prepubertal girl
  • Pale moist appearance of pubertal vaginal mucosa, elongated clitoris
  • Labia minor more visible as puberty progress

Evidence of gonadotropic stimulation

  • Measure phallic and testicular dimension: testicles must be =
  • Without testicular enlargement, penis enlargement, adrenal pathology
  • Testicular volume is greater than phallic size in normal puberty, CPP, and Primary hypothyroidism

Pseudoisosexual precocious puberty

Penile dimension are disproportionately greater than testicular size

67
Q

LAB TESTING FOR PP

A

Further evaluation should be directed at the possibility of:

  • Nutritional disorders
  • Occult chronic illness
  • Hormonal abnormalities

Initial screening should include:

  • Complete blood count
  • Erythrocyte sedimentation rate
  • Liver function tests
68
Q

LAB TESTING FOR PP If hypothyroidism is suspected…

A

Thyroid hormone should be assessed TSH, free T4 is vital If growth abnormality is found, do a bone age OF LEFT WRIST

69
Q

The Hormonal eval for PP should include the following tests

A

Random serum LH and FSH Estradiol (females)/testosterone (males) should be obtained to distinguish between primary and secondary hypogonadism

70
Q

Precocious puberty: Stature

A

Sexual precocity is more common in girls than boys.

In both cases, linear growth is accelerated during childhood, often with markedly advanced bone maturation.

Because of very early epiphyseal closure, the paradoxically tall child will be short as an adult

71
Q

SUMMARY – Females

A

No Menarche 5 years after breast development

No Menses by age 16 years ( Primary Amenorrhea)

Over 50% of delayed puberty is due to constitutional delay (late bloomers)

72
Q

Summary of Puberty findings

A

Historical clues

Physical findings

Selected lab values

Treatment Males = testosterone Females = estrogen

73
Q

Three Major Patterns in Infants and Children

A

Normal head circumference, normal height and decreased weight initially and eventually decelerating ht and head as well. (Type 1)

Normal head circumference, disproportionate height and almost normal weight (type 2)

Small head circumference and decreased weight and height (type 3)

74
Q

Type 1

A

Retardation of weight with near normal or slowly decelerating height and HC Suggests under nutrition

75
Q

Type 2

A

Near proportional retardation of weight and height with normal HC

  • Constitutional growth delay
  • Genetic short stature
  • Endocrinopathies
  • Structural dwarfs
76
Q

Type 3

A

Concomitant retardation of weight height and HC

SGA: in utero and perinatal insult

Chromosomal aberrations

CNS abnormalities

Rarely familial

77
Q

Normal Upper segment to lower segment ratio

A

Upper segment head to symphysis pubis to lower segment (type 2)

US to LS in infants is 1.7 to 1.8 to 1

As child approaches adolescent .9 to l.0:1

Upper: lower segment ratio is low in Marfan syndrome

Abnormal in bony dysplasia

After spinal irradiation

78
Q

Growth curve

A

Deceleration of linear growth in a well-nourished child

  • Growth hormone deficiency
  • Hypothyroidism
  • Glucocorticoid excess (causes Cushing’s syndrome)

Initial decline in weight followed by decreased height velocity Malnutrition or systemic illness.

Dysmorphic features Chromosomal abnormality (Trisomy 21 or Turner s syndrome) or other specific syndrome

Disproportionate features or skeletal abnormalities Consistent with skeletal dysplasia or metabolic bone disease.

79
Q

Eval of Attenuated Growth

A

Careful physical exam Free T4, TSH ESR Electrolytes, BUN creatinine, UA, LFT

Bone age of left hand and wrist

Markedly delayed bone age suggestive of endrocrinopathy Refer to endocrine

80
Q

Accelerated Growth Differential Dx

A
  • Upward crossing of percentiles of concern
  • Over-nutrition most common cause – weight affected and more severely than height
  • Differential diagnosis
    • Precocious puberty (adrenal or gonadal)
    • Hyperthyroidism
    • Genetic (familial) or syndrome (Klinefelter or Marfan’s)
    • GH excess
    • Development of pubic hair
81
Q

Short Stature (5)

A

Normal Patterns of Growth

  • Familial or genetic short stature
  • Constitutional Growth delay

Primary growth disturbance

  • Intrauterine growth retardation

Systemic illness

Genetic disorders

  • Chromosomal defects: Turner syndrome, Down syndrome Syndromes: Noonan, Prader Willi, Russell Silver Syndrome

Disproportionate short stature

  • Skeletal Dysplasia
  • Spinal irradiation

Most commonly familial or due to constitutional growth delay or comb

May rarely be associated with serious underlying medical condition

82
Q

WHEN TO WORRY ABOUT GROWTH

A

Abnormally slow growth rate

Downward crossing of percentile channels on the growth chart after age 18 mo.

Height below the 3rd percentile

Height significantly below genetic potential by 2 SD

83
Q

SHORT stature EVAL (6)

A

Do a careful prenatal history with birthweight

  • IUGR is birth weight less than 10th percentile for gestational age

Look at growth points

Look at growth velocity

Determine parental height, do mid-parental height

For constitutional growth delay, do bone age

  • Slow growth during the first two to three years with normal or low normal annual growth after
  • History is similar in family member

Look at weight to ht ratio : If decreased systemic illness

84
Q

TURNER SYNDROME (8)

A

Multiple nevi

Low posterior hairline

webbed neck

Broad chest with wide spaced nipples

Short 4th metacarpals

Coarctation of the aorta with bicuspid aortic valve

Increased carrying angle of arms or CUBITUS VALGUS

50% have sleep apnea

85
Q

Causes of short stature

A

Normal pattern of growth

Familial or genetic short stature

Constitutional growth delay

Primary growth disturbance

Intrauterine growth retardation

Genetic disorders

Disproportionate short stature

86
Q

Systemic Illness associated with short stature

A

Systemic illness

  • Hypocaloric Malnutrition
  • GI
  • Poorly controlled DM

Metabolic Renal Hepatic Cardiac Hematologic Respiratory (CF, severe asthma) Chronicinfection

Endocrine disorders

  • Hypothyroidism
  • Cushing’s syndrome: Glucocorticoid excess (endogenous or exogenous)

Growth hormone deficiency

  • Isolated, multiple
87
Q

Abnormally rapid growth velocity

A

In general, a child whose height differs by more than 2 standard deviations (SD) from the population mean is considered too tall.

Although tall stature is as common as is short stature, few children or their families seek medical attention, presumably because tall stature is socially acceptable and often advantageous.

88
Q

THE MAINSTAYS OF ASSESSMENT OF TALL OR RAPIDLY GROWING CHILDREN INCLUDE:

A

The child’s pattern of growth

Medical History

Physical Exam

89
Q

Stature overgrowth – dysmorphic features found need to…

A

When dysmorphic features are found, special effort should be made to rule out syndromes that are associated with excessive growth.

Stature in overgrowth = infancy and adolescence

90
Q

Overgrowth in infancy

A

Maternal DM

Cerebral Gigantism

Beckwith-Wiedemann Syndrome

91
Q

Maternal Diabetes Mellitus

A

Maternal DM is the most common cause for LGA in infants

These infants usually are large, more so in weight than in length

92
Q

Cerebral Gigantism (Soto’s Syndrome) Assessment (7)

A
  • Infants with cerebral gigantism tend to be large at birth and continue to grow rapidly during the early years of childhood.
  • High forehead
  • Frontal bossing
  • Hypertelorism
  • Prominent jaw
  • High arched palate
  • Mental retardation poor concentration
  • Adult height is normal in many of these infants
93
Q

Beckwith-Wiedemann Syndrome

A

Macrosomia

Visceromegaly

Macroglossia

Omphalocele

Prominent occiput Hypoglycemia with hyperinsulinism

The cause of this syndrome is unknown, but increased production of IGF-2 may explain the overgrowth.

94
Q

Overgrowth in Childhood and adulthood Non-Endocrine Disorders

A

Non-Endocrine Disorders

Familial (Constitutional) Tall Stature

Exogenous Obesity

Precocious Puberty

Marfan Syndrome

Homocystinuria

Neurofibromatosis Type 1

95
Q

Overgrowth in Childhood and adulthood Endocrine Disorders

A

Growth hormone excess

96
Q

Non-endocrine disorders familial (Constitutional) Tall stature

A

Familial tall stature is a variant of the normal pattern of childhood growth.

Height is 2 SDs above the corresponding mean height for age and gender.

Genetic factors play the most important roles in the pathogenesis of familial tall stature.

Growth hormone secretion and serum IGF-1 and IGF binding protein-3 concentrations often are in the upper range of normal.

97
Q

Exogenous obesity

A

OBESITY MAY BE ACCOMPANIED BY MODEST LINEAR OVERGROWTH AND EARLY ONSET OF PUBERTY

These children usually have diminished overall growth hormone production but high normal serum concentrations of growth hormone- binding proteins and IGF-1

Due to Leptin increase, may have upper limit TSH Bone age may be advanced and puberty starts early, causing premature epiphyseal fusion

98
Q

Gigantism

A

Excessive linear growth that occurs with growth hormone (GH) excess when epiphyseal growth plates are open during childhood

99
Q

Acromegaly

A

Disorder of GH excess in adulthood

100
Q

Tall Stature Summary

A

Growth velocity is the best way to assess a child whose height > 2 SD.

Dysmorphic features and developmental delay may suggest a non-endocrine cause of tall stature.

Although rare, growth hormone excess should be considered if the growth velocity is accelerated + a family history of MEN 1.

Transsphenoidal removal of the pituitary adenoma, when present, offers definitive treatment of growth hormone excess.

101
Q
A

PNP: Physical Assessment - BK (13 decks)

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