Lecture 23: post-natal growth Flashcards
Abnormal growth can be caused from?
Genetic disorders
Endocrine disorders
Cartilage or bone disease
General chronic disease
Phases of Growth?
Infant - rapid growth a birth declining over 2 years (less GH dependent)
Childhood - Constant anual growth (GH dependent)
Puberty - Rapid growth primarily dependent on sex steroids and increase GH release
Mid-parental height?
An estimate to the height potential based on the parents heights
boys: (dad’s + (mum’s - 13cm))/2
girls: ((dad’s -13cm) + mum’s)/2
Useful height range and is +/- 8cm
What is height velocity?
- HV differentiates normal variant short stature from pathological short stature
- Ideally calculated of 6-12 months and is calculted by dividing the height gain by the time interval between the two
- Normal HV lies between 25-75th percentile, the curve is shaped differently in children with delayed or early puberty.
Short Stature?
- A common clinical presentation - a symptom or a variant and not a disease
- May indicate pathology BUT normal short stature still grow with normal HV
- Common manefestation of chronic illness
Growth disorders?
Normal HV: Normal variants
- Familial short stature
- Constitutional delay in growth and development
Poor height velocity: Usually pathological
- Proportionate/disproportionate
Bone Age?
Looks at the ‘age of the bones’ and used to predict adult height
Hand used (with lots of long bones) in X-ray looking at the formation of the bones - very hard to do.
FSS vs CDGD
birthweight, chronic ilness, family Hx, infant growth, childhoodgrowth, late childhood growth, bone age, puberty and final height?
Puberty = ontime, delayed
Final height = short, normal
Importance of:
ACTH, AVP, GH, TSH, Adrenal, Prolactin, Ocytocin, LH/FSH ?
ACTH: death
AVP: dehydrated
GH: severly short
TSH: short and slow
Adrenal: death
Prolactin: no food
Ocytocin: No labour
LH/FSH: No gonadal function
Growth Hormone secretion? Nutrition and the GH axis?
Pulsatile with low baseline
Primarily at night time
Increased by: sleep, exercise, stress, hypoglycaemia, amino acids
Decreased by: obesity, psychosocial deprivation
GH causes the liver to make IGF-1 that then negatively inhibits GH release. In malnourished kids the liver doesn’t produce enough IGF-1
GH actions?
Metabolic:
- inhibits glucose uptake and promotes glycogenolysis (anti-insulin)
- Stimuates protein synthesis
- Promotes lipolysis
ACTS: endocrine, paracrine, autocrine
- Bind to GH receptors on the perichondrocytes causeing IGF-1 release
Role of IGF-1?
- Major post-natal growth promoting factor -(majority bound to binding proteins)
- Principally produced in the liver (endocrine) and bone (para, autocrine) acting on a wide range of tissues
- Insulin-like (promoting glucose, lipid and amino acid uptake) = cell proliferation and differentiation.
Estrogen?
- Effects on skeleton and body composition (more so than testosterone on skeleton)
- responsible for epiphyseal maturation/closure in both sexes
Thyroid hormones? Insulin?
T3 and T4 - facilitatory role in growth
necessary for normal GH secretion and growth plate development
Insulin - Facilitatory role in growth providing substrate for growth (aa uptake, glycogenesis and lipogenesis)
GH at fetal, infant and child levels?
Fetal = IGF-1 and insulin
young children = GH, IGF-1, T3/4
Puberty = Inc. GH, IGF-1, E2/T, Insulin and same T3/4 levels
