Week 7/8 physiology

Growth bones/aging, Skin burns and wound healing.

What is growth?

Increased length of long bone and increased size of number of cells in soft tissue.

What factors influence growth?

Genetics, diet, hormones

What stunts growth?

Malnourishment and cortisol

How are hormone levels controlled

Primary GH and sex hormones during puberty

where is GH secreted and how is it controlled? and what does the hypothalamus release

Secreted at the anterior piturity and controlled by the hypothalamus releasing- Growth hormone releasing hormone (stimulates growth), and growth hormone inhibiting hormone) slows growth down

Why does GH have both "metabolic" and "growth" effects, and what's the difference?

Metabolic effects = GH acts directly on tissues to regulate fat/glucose use. Growth effects = GH stimulates the liver to make IGFs, which then mediate actual tissue growth (indirect).

When is GH secretion highest, and what else triggers its release?

Highest during deep sleep (diurnal pattern). Also triggered by exercise, stress, and low blood glucose — situations where the body needs to conserve glucose and mobilize alternative fuel.

What triggers GH release?

Falling/low blood glucose (exercise, stress, and low blood sugar all trigger this).

What are GH's two metabolic effects on blood glucose?

Burns fat instead of glucose, and blocks tissues from taking up glucose — keeping more glucose in the blood.

Why does GH do this?

To conserve glucose for the brain.

What's the difference between GH's metabolic effects and growth effects?

Metabolic = GH acts directly, fast. Growth = GH → liver → IGFs → growth (indirect, slower).

What shuts off GH release (negative feedback)?

Rising IGF levels signal the hypothalamus to release less GHRH and more GHIH.

How does GH promote growth in soft tissues?

Increases cell number (hyperplasia) and cell size (hypertrophy).

How does GH promote growth in bones?

Increases bone thickness and bone length.

Where do long bones grow?

At the epiphyseal (growth) plate — made of hyaline cartilage.

What happens to the growth plate at puberty?

It closes (due to sex hormones) — while open, bones can grow; once closed, they can't anymore.

How does bone lengthen at the growth plate?

Cartilage cells (chondrocytes) divide and grow, then calcify and get replaced by bone.

What does GH do overall (summary)?

1) Releases triglycerides into blood, 2) thickens bones, 3) causes hyperplasia & hypertrophy in soft tissue, 4) promotes bone lengthening.

What causes dwarfism, and what's the difference from acromegalic dwarfism?

Pituitary dwarfism = not enough GH released (or GH receptors don't work — Laron dwarfism), but body stays proportionate. Acromegalic dwarfism = limbs haven't grown to their full potential (disproportionate).

What does too much GH cause in children vs adults?

Children = gigantism (excessive long bone growth, very tall). Adults = acromegaly (bones already fused, so bones thicken and soft tissue grows instead).

What are signs of acromegaly?

Big forehead, growth of nose/jaw, thickening bones and soft tissue.

what us •Haematopoiesis

production of blood cells

What are the two types of bone tissue?

Trabecular (spongy) bone and cortical (compact) bone.

Where is compact bone vs spongy bone located?

Compact bone = diaphysis (shaft) of long bone. Spongy bone = center of epiphysis (ends).

What are trabeculae?

Small "beams" that make up the structure of spongy bone.

What gives bone its hardness vs flexibility?

Mineral salts (inorganic, ~65-70%) = hardness. Osteoid/collagen fibers (organic, ~30-35%) = flexibility. Together = durability & strength.

What happens if you remove the organic part vs inorganic part of bone?

Remove organic (collagen) → bone becomes brittle, shatters easily. Remove inorganic (minerals) → bone becomes very flexible, can't bear weight.

What are the 3 main bone cells and their jobs?

Osteoblasts = build bone (secrete osteoid). Osteoclasts = break down bone (release calcium). Osteocytes = sense mechanical changes, embedded in bone.

Walk through the RANKL pathway.

Osteoblasts secrete RANKL → binds RANK on macrophages → macrophages turn into osteoclasts + survive longer → osteoclast activity ↑ → bone breakdown outpaces building → bone mass ↓

Walk through the OPG pathway.

Osteoblasts secrete OPG → OPG binds up RANKL so it can't attach to RANK → osteoclast formation blocked → osteoclast activity ↓ → bone building outpaces breakdown → bone mass ↑

What controls bone remodeling hormonally, and what's the main stimulus?

PTH (parathyroid glands), Vitamin D, Calcitonin (minor role). Main stimulus = change in blood Ca²⁺.

Walk through the PTH feedback loop.

Blood Ca²⁺ drops → stimulates parathyroid glands → releases PTH → acts on bone, kidney, intestine → raises blood Ca²⁺ → rising Ca²⁺ inhibits further PTH release (negative feedback)

How does PTH raise blood Ca²⁺, and what are the two mechanisms?

Takes calcium out of bone storage. Fast exchange = immediate regulation. Slow exchange = breaks down bone, response to chronic low calcium.

How does fast exchange of Ca²⁺ work?

PTH activates pumps that move Ca²⁺ straight from bone fluid into blood (via central canal). Quick, and bone-sparing (no bone broken down).

How does slow exchange of Ca²⁺ work?

Happens with chronic low blood Ca²⁺. PTH inhibits osteoblasts → they secrete RANKL → activates osteoclasts → osteoclasts break down bone → releases Ca²⁺ and phosphate into blood.

What does PTH do at the kidneys and intestines?

Kidneys — pulls Ca²⁺ back into blood (less in urine), also activates vitamin D. Intestines — vitamin D (activated by PTH) increases Ca²⁺ absorption from food

How does mechanical load/strain relate to bone mass?

Too little load (disuse, e.g. immobilization or antigravity) → osteoclasts ↑, osteoblasts ↓ → bone resorption → bone mass decreases.

What happens when load/strain goes above the normal range (e.g. exercise)?

Shift toward bone formation — osteoblasts ↑, osteoclasts ↓ → increased bone mass.

What type of exercise increases bone mineral density most?

Load-bearing, high-impact sports (e.g. weightlifting, football, soccer)

What is osteoporosis?

Reduced bone mineral density → weaker bone → higher fracture risk. Progresses: normal → osteopenia → osteoporosis

When is peak bone mass reached, and how does it differ by sex?

Peak bone mass around age 30. Men reach higher peak bone mass than women.

Why does menopause increase osteoporosis risk?

Oestrogen normally boosts OPG, which inhibits osteoclasts. At menopause, oestrogen drops → osteoclast activity increases → more bone resorption → bone loss. (Same logic applies to men with low testosterone, since testosterone converts to oestrogen.)

What are the risk factors for osteoporosis, and which are modifiable?

Poor nutrition, sedentary lifestyle, low oestrogen/testosterone, smoking/alcohol/caffeine, being over/underweight, low sun exposure, corticosteroid use. Modifiable ones: diet, exercise, sun exposure.

How can osteoporosis be prevented?

Increase peak bone mass early (good nutrition + weight-bearing exercise before age 30), maintain calcium/vitamin D, and keep exercising in older age (reduces bone loss, prevents falls/fractures).