AGE REVISION PART 2 Flashcards
- What is the difference between trobecular and cortical bone?
- Cortical (compact) bone
- Trabecular (spongy, cancellous) bone
- Cortical bone is much denser and is found primary is found in the shaft of long bones and forms the outer shell around cancellous bone at the end of joints and the vertebrae. Trabecular bone is much more porous.
- What are osteoblasts, osteoclasts, osteocytes and osteiod?
osteoblasts are bone forming cells.
osteoclasts are bone reabsorbing cells.
osteocytes are communication cells from osteocytes to surface cells and systemic circulation.
Osteoid is the organic matrix of the bone.
- What is the role of osteocytes and what system is this done by?
Lacunar-Canalicular network: Allows communication between osteocytes and from osteocytes to surface cells and systemic circulation. They do this to regulate bone remodelling in response to mechanical and endocrine stimuli
osteocytes regulate bone remodelling in response to mechanical and endocrine stimuli. Which factors favour bone formation and which factors favour bone reabsorption?
Factors favouring resorption
• Unloading (bedrest, zero-gravity, etc)
• Lack of activity/ less stress in on the bone will cause bone density to decrease.- causes bone reabsorption
Factors favouring formation
• Load-bearing exercise
• On the contrary load-bearing exercises causes bone formation. – this is ordinary load bearing exercises could just be walking
what is RANK, RANK ligad and OPG?
- RANK (receptor activator of nuclear factor kappa-B): surface receptor on pre-osteoclasts, stimulates osteoclast differentiation (rank is the receptor)
- RANK-ligand: produced by pre-osteoblasts, osteoblasts and osteocytes; binds to RANK and stimulates osteoclast differentiation (rankl is the ligand for this receptor)
- OPG (osteoprotogerin): decoy receptor produced by osteocytes; binds to RANK-L, preventing activation of RANK (binds to the receptor stops rankl from binding
what is the role of sclerostin in bone formation?
essential negative feedback on bone formation. Its absence results in excessive bone formation. It’s of particular interest since intervention in sclerostin expression can alter the balance between bone formation and bone resorption. It’s a brake on bone formation, and mechanical stress can take this brake off.
what is the difference between Osteoporosis and osteomalacia
Osteoporosis: loss of bone mass. loss of bone mass both mineral density and organic matrix. Osteoporosis is generalised imbalance, in the direction of resorption
Osteomalacia: loss of bone mineralization. makes bones soft – lack of vit d and sun.
what is the role of parathyroid hormone and Vitamin D in bones?
- Increases Ca absorption from gut
* Synergistic effects with PTH on bone
what is the role of calcitonin in bones?
- Negative feedback regulation of serum Ca
- Released in response to rises in Ca
- Inhibits osteoclast function
what are the actions of oestrogen on bones?
- Regulates life cycle of osteoblasts and osteoclasts
- Osteoclasts: shorten (promote apoptosis)
- Osteoblasts: lengthen (protect from apoptosis)
- Indirectly inhibit osteoclast differentiation
- May be necessary for new bone formation in response to mechanical stress
What is Frailty?
A: An inevitable consequence of ageing
B: A state due to multiple long term conditions
C: A condition in which the person becomes fragile
D: A state associated with low energy, slow walking speed, poor strength
E: A condition for which nothing can be done
D
Frailty is a state of increased vulnerability- due to poor resolution of homoeostasis after a stressor event, which increases the risk of adverse outcomes, including falls, delirium, and disability
what are some of the Pathophysiologies of frailty
- Decline across all body systems with ageing
- In frailty this decline in function is accelerated/ more marked
- Loss of homeostatic mechanisms
- Reduction in VO2 max-
- Reduction in maximal HR
- Reduced resting metabolic rate
- Neuroendocrine changes- increased cortisol, decreased GH, vitamin D
- Reduced appetite
Sarcopaenia is a key component of frailty syndrome , what is it?
Sarcopeniais the degenerative loss of skeletal muscle mass quality, and strength associated with ageing.
explain the link between frailty and chronic inflammation
- Association between frailty and elevated circulating levels of interleukin (IL)-6
- C-reactive protein, and tumour necrosis factor-α, have also been shown to Have elevated levels in frail older adults.
- Chronic inflammation may directly contribute to certain parts of the frailty phenotype e.g sarcopenia.
How is frailty diagnosed?
Dynanometer
- For testing grip strength
Frailty Phenotype – Fried 2001 - Unintentional weight loss - Reduced muscle strength - Reduced gait speed - Exhaustion -Sedentary behaviour Those with 3 or more are said to have frailty
Cumulative Deficit Model (Rockwood 2005) 32 baseline variables -Signs e.g. tremor -Symptoms e.g low mood -Disease states -Abnormal laboratory values -Disabilities Calculation to create score
- The more individuals have wrong with them, the more they are likely to be frail
- Allows frailty to be gradable, rather than present or absent
Clinical Frailty Scale- scale that ranges from very fit to terminally iill
Edmonton Frail Scale
Electronic Frailty Index – Clegg 2016
The ‘prisma 7 questions