Growth is not just "getting bigger." It reflects the integrated function of genetics, hormones, nutrition, organ systems, and psychosocial well-being. A child who stops growing or deviates from their expected trajectory is essentially telling you something is wrong—long before other symptoms appear. This is why serial plotting on growth charts is the single most important surveillance tool in paediatrics.

Growth is an orchestrated network of control—it cannot be too much, cannot be too little, and must happen at the right time and right place. ^[1]

Size is determined by:

1. Genetic potential – parental heights set the "target"
2. Hormonal milieu – GH, thyroid hormone, sex steroids, cortisol, insulin/IGF-1
3. Nutrition – calories, protein, micronutrients
4. Health/disease – chronic illness diverts energy from growth
5. Psychosocial environment – deprivation and stress suppress GH secretion

Why this matters: In the fetal phase, genetics play a smaller role than maternal/placental factors—a large genetic father can have a small baby if the mother is small or malnourished. After birth, the child "catches up" or "catches down" to their genetic potential over the first 2 years. After age 2, deviation from centiles is more concerning because growth should be tracking steadily.

Normal growth is the progression of changes in weight, height, and head circumference that are compatible with established standards for a given population, reflecting genetic potentials and environmental factors, with adequate lengthening of the skeleton. ^[1]

A newborn's size is determined by the intrauterine environment—influenced by maternal size, nutrition, general health, and social habits (e.g., smoking status). ^[1]

This is why birth weight correlates more with maternal size than paternal size. A genetically tall baby born to a small mother will be constrained in utero but will "catch up" postnatally.

Growth velocity is greatest in late fetal life, then peaks again during puberty, and eventually decreases when oestrogen-mediated epiphyseal fusion occurs in adolescence. ^[1]

Key point: It is oestrogen (not testosterone) that causes epiphyseal fusion in both sexes. Boys grow taller than girls partly because they enter puberty ~2 years later, giving them more years of pre-pubertal growth at ~5 cm/year.

Growth rates are similar between genders until puberty. Males have a later pubertal growth spurt and higher velocity during the spurt. ^[1]

Hong Kong-specific data (exam-worthy):

50th centile adult height: Male = 171 cm, Female = 158 cm in Hong Kong. ^[1]

Average length at birth for a term infant is 50 cm (20 inches). ^[1]

Children reach one-half of their adult height by 24 to 30 months. ^[1]

This is a useful clinical rule. Example from the lecture: Ethan is 86 cm at 24 months → predicted adult height ≈ 86 × 2 = 172 cm.

Boy = (father's height + mother's height + 13) ÷ 2 Girl = (father's height + mother's height − 13) ÷ 2 ^[1]

The ±13 cm adjusts for the average height difference between adult males and females. The target range is MPH ± 8.5 cm (approximately 3rd to 97th centile for that family).

Example from lecture:

Ethan: Mother 164 cm, Father 170 cm → MPH = (164 + 170 + 13)/2 = 173 cm ^[1]

Though not heavily detailed in this lecture, head circumference is the third key growth parameter. It reflects brain growth. In failure to thrive, weight drops first, then height, with relative sparing of head circumference (the body protects brain growth). If head circumference is disproportionately affected, think of a primary neurological/genetic problem rather than nutritional failure.

Short stature is defined as a height that is 2 standard deviations (SD) or more below the mean height for individuals of the same sex and chronologic age in a given population. This translates to a height below the 2nd percentile. ^[1]

Note: Some sources use the 3rd percentile as the cutoff. The lecture uses 2nd percentile (= −2 SD). For the exam, go with the lecture definition.

1. How short is the child? 2. Is the child's height velocity impaired? 3. What is the child's predicted adult height? ^[1]

Height velocity is more important than a single height measurement. A child on the 5th centile who is growing at a normal velocity along that centile is likely a normal variant. A child on the 25th centile whose growth is crossing downward is more concerning.

P – Psychological deprivation I – Iatrogenic (glucocorticoids, spinal radiation) C – Chronic illness N – Nutritional I – IUGR (unknown aetiology or part of a syndrome, e.g., Russell-Silver syndrome) C – Chromosomal (Turner, Noonan, Down, Prader-Willi) S – Skeletal dysplasia (achondroplasia, hypochondroplasia) ^[1]

Plus Endocrine causes: hypothyroidism, GH deficiency, Cushing syndrome.

This is the lecture's core clinical classification and is extremely high-yield:

1. Dysmorphism with a recognizable syndrome 2. Disproportionate short stature – usually needs a skeletal survey 3. Short but thin – search for chronic illness 4. Short and fat – more suggestive of an endocrine cause ^[1]

Body height < 1st centile; abnormally short for family heights; history or examination suggestive of chronic illness; abnormal growth velocity; abnormal body proportions; dysmorphic features or midline defects. ^[1]

Search for associated chronic disease: cardiovascular disease, respiratory disease (cystic fibrosis), malabsorption/chronic inflammatory bowel disease, chronic renal failure, psychosocial deprivation, anorexia nervosa. ^[1]

Also: rickets (chronic renal failure → vitamin D deficiency → poor bone mineralization) and thalassaemia (chronic anaemia, iron overload, endocrine dysfunction from haemosiderosis).

Why short AND thin? The chronic illness consumes energy reserves → weight drops first (thin), then linear growth suffers (short). This is the opposite pattern to endocrine causes.

More suggestive of endocrine cause: panhypopituitarism, isolated growth hormone deficiency, hypothyroidism, pseudohypoparathyroidism, Cushing's syndrome, Prader-Willi syndrome. ^[1]

Why short AND fat?

• GH deficiency: GH promotes lipolysis and linear growth. Without it, fat accumulates and bones don't grow.
• Hypothyroidism: Thyroid hormone is essential for normal bone maturation and metabolism. Low TH → slow metabolism (fat gain) + delayed bone age (short).
• Cushing's syndrome: Excess cortisol promotes central adiposity and inhibits GH secretion and growth plate activity.
• Prader-Willi syndrome: Hyperphagia from hypothalamic dysfunction + GH deficiency → extreme obesity with short stature.

Two normal variants: Familial short stature and Constitutional delay. ^[1]

• Tall parents, may have family history of early puberty
• Bone age may show advancement → helps predict final height

Hyperthyroidism; Precocious puberty (tall at diagnosis but reduced final height due to premature fusion of epiphyses); GH-secreting tumours (extremely rare in paediatrics). ^[1]

Why is precocious puberty a cause of TALL stature initially but SHORT final height? Early puberty → early sex steroid exposure → early growth spurt (child is temporarily tall for age) → but also early epiphyseal fusion → growth stops prematurely → reduced adult height.

BMI is the widely accepted standard measure of overweight and obesity for children ≥ 2 years. ^[1]

Adult WHO cut-offs:

Overweight: BMI > 25 (Asian > 23); Obesity: BMI > 30 (Asian > 25) ^[1]

Paediatric definition (age- and sex-specific BMI charts):

Overweight: ≥ 1 SD above mean BMI for age and sex Obesity: ≥ 2 SD above mean BMI for age and sex ^[1]

Note: In children, absolute BMI numbers change with age, so we use centiles/SD scores on age-sex-specific BMI charts rather than fixed thresholds.

Genetics/Epigenetics, Early life events, Biology, Environment, Stress, Behaviour ^[1]

Most childhood obesity is exogenous (energy intake > expenditure). Endocrine/genetic causes (e.g., hypothyroidism, Cushing, Prader-Willi) are rare but must be excluded if the child is also short—remember the "short and fat" group points toward endocrine pathology.

Metabolic syndrome prevalence: normal weight adolescents 0–4.7% vs obese 14.5–35%; 1/3 of children with NAFLD had T2DM or prediabetes; Adolescents with severe obesity may have more advanced liver damage than adults; Pediatric T2DM has more rapid β-cell failure than adults; Obese young-onset T2DM has very high mortality rate. ^[1]

1. A 5-year-old girl is found to be below the 2nd centile for height. She has a webbed neck, shield chest, and wide-spaced nipples. What is the most likely diagnosis? → Turner syndrome (karyotype 45,X)

2. A child is short and overweight with delayed bone age. What is the most likely category of cause? → Endocrine (short and fat)

3. What investigation must be performed in ALL girls with unexplained short stature? → Karyotype

4. By what age do infants double their birth weight? → 4 months. Triple? → 1 year.

5. A 2-year-old boy is 86 cm. What is his estimated adult height? → 86 × 2 = 172 cm

2016 Q10: "What parameters obtained during physical examination could be used as an indicator of the general well-being of a child?" ^[8]

• Answer: Weight, height/length, head circumference, BMI, body proportions, growth velocity (serial measurements on growth chart), pubertal staging, nutritional status, dysmorphic features assessment

Possible SAQ: "A 10-year-old girl is referred for short stature. Height is below the 1st centile. Parents are of normal height. Outline your approach."

• Markscheme: History (pregnancy, birth weight, growth velocity, nutritional, family heights/MPH, systems review, psychosocial); Examination (accurate measurements, proportions, dysmorphism, midline defects, visual fields, thyroid); Investigations (CBP, ESR, LFT, RFT, electrolytes, bone profile, TFT, IGF-1, bone age, KARYOTYPE); Classify into 4 groups; Manage underlying cause; Refer to paediatric endocrinologist.