Growth & Growth Hormones Flashcards
relative growth with age of the brain, total-boy height, and reproductive organs
- Brain → Rapid growth early in childhood years - about 10 almost 100% growth
- total-body height → Growth of vertical skeleton including long bones which once it reaches its peak does not continue to grow
- reproductive organs → Does not take off until adolescence and then rapid growth
Human growth of girls vs. boys
girls typically sooner than boys
What is the postnatal growth spurt?
first 2 years a dramatic increase in height and weight than growth continues but slower
WHat is the puberty growth spurt?
A major growth spurt happens at the time of puberty, usually between 8 to 13 years of age in girls and 10 to 15 years in boys. Puberty lasts about 2 to 5 years.
- When adolescence growth stops then no further height is possible
what is vertical growth associated with?
long bone growth
- arms → humerus and radius
- legs → femur, tibula and fibula)
- collarbone
Long bone anatomy
- epiphysis → the head of the long bone and fits into socket or articulates with another bone
- composed of spongy bone and has red bone marrow
- Shaft → long part of the bone/ middle of the bone between the epiphysis ends
- composed of compact bone and cavity is lined with this vasculature and filled with yellow bone marrow
- Epiphyseal plate → cartilage between epiphysis and diaphysis
What is the target site for linear growth in the long bones?
The epiphyseal plate is site of growth in length of bone because it has cartilage not bone and it has the target cells for the action of GH and IGF-1:chondrocytes
What are the 3 specialized bone types?
- osteoblasts
- osteoclast
- osteocyte
Osteoblasts
Bone makers
- provide collagen and proteoglycans to make the osteoid matrix
Purpose of collagen and proteoglycans in bone
- Collagen → provide strength
- proteoglycan → makes collagen more resistant by trapping water
Osteoclast
Bone breakers → responsible for resorption or breakdown of bone
- Secrete acids and enzymes that break down bone material. The acids dissolve down the calcium phosphate crystals that make the calcified matrix of bone and enzymes help degrade osteoid that was laid down. Calcium and phosphate can then be released into blood coming from the bone
Osteocyte
Bone maintainers
- osteoblasts that are surrounded by bone matrix after being calcified
- Can have long cell processes that can connect with each other and they do this to serve the purpose’s function of keeping tabs on status for the bone.
- Can direct activities of osteoclasts
BY weight mature bone matric consists of..?
- 35% organic (collagen & proteoglycans) → osteoid
- 65% inorganic (calcium phosphate crystals = hydroxyapatite) → minerals
What happens to bone without minerals/ collagen?
- Without minerals → collagen (organic) is the primary constituent and bone is overly flexible
- Without collagen → mineral (inorganic) is the primary constituent and bone becomes very brittle
What are chondrocytes?
the cellular component of cartilage and thus the target cells of GH
Bone Growth
- GH can stimulate both, directly and indirectly, the 2 processes of growth which are hypertrophy and hyperplasia.
- GH can stimulate chondrocyte differentiation, the chondrocytes are the target cells
- IGF-1 stimulated by GH can stimulate growth of chondrocytes via cell division.
- IGF-1 can come from the liver and can be locally released from bone and effect is demonstrated as chondrocyte increase in size (hypertrophy) as well as increasing in cell numbers (hyperplasia).
Result forms expanding layer of cartilage and overall plate growth occurs and becomes longer and taller. Meanwhile, osteoblasts found in the regions of the boundary between shaft and plate are visibly making new bone with osteoid by replacing the chondrocyte. The osteoblast gradually build up new bone and permanently lengthens the bone adding to the shaft
What occurs with a bone fracture?
- Hematoma → After a fracture, blood escapes from ruptured bone producing hematoma (~8 h); Around the fracture site and secretion of cytochines and recruits immune cells for bone repair.
- Fibrocartilaginous callus → Tissue repair begins with fibrocartilaginous callus forming in between the ends of the broken bone (~3 wks); stem cells recruit and differentiate to bone cell types and form a collagen-rich mesh across so layers of spongy bone get laid down
- Bony callus → Osteoblasts produce trabeculae of spongy bone and convert the fibrocartilage callus to a bony callus, joining broken bones and newly formed blood vessels grow leading to immature bone (~3 mths)
- Remodelling → Osteoblasts build new compact bone at the periphery, and osteoclasts absorb the spongy bone, creating a new medullary cavity
Growth Hormone feedback system
- GHRH stimulates anterior pituitary GH release
- SST (somatostatin) inhibits anterior pituitary GH release (GHIH)
Overall summary of growth hormone
Increased GH effect on liver
Increased GH effect on general tissues
-
physiological response:
- increased protein synthesis in muscle
- increased insulin-like growth factor secretion
- Result: provide energy and substrates for growth
Increased GH effect on adipose tissue
-
physiological response:
- decreased glucose uptake: Decreases amount of glucose that fat tissue takes up and leaves more glucose in circualtion
- increased lipolysis: Triglycerides are broken down so FA and glycerol are released into circulation
- Result: provide energy and substrates for growth
Increased GH effect on muscle
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physiological response:
- decreased glucose uptake: Inhibit glucose uptake by muscle leaving more in bloodstream to be used as fuel for other cells hence can provide energy and substrates for growth
- increased amino acid uptake: muscle growth
- Result: provide energy and substrates for growth
Effects of a growth hormone- secreting tumor
Lead to secretion of more GH so high levels in circulation and high levels will effect metabolic tissue and lead to increase in blood glucose levels. Hence because of tumour might have hyperglycaemia. Many metabolic effects of GH are opposite to IGF-1. Can also effect liver and stimulate IGF-1 so more in blood which stimulate growth promoting effects. High levels if IGF-1 will mean more negative feeedback of hypo so inhibit GHRH and stimulate SST. GH also has the short loop negative feedback to support this. High levels of IGF-1 normally inhibits ant pit cells so they secret less hormone which remains true however the negative feedback does not go to the tumour so GH levels continue to be secreted in the blood. So despite negative feedback loop it continues to be secreted by tumour
