AGE REVISION PART 2 Flashcards

1
Q
  • What is the difference between trobecular and cortical bone?
A
  • 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.
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2
Q
  • What are osteoblasts, osteoclasts, osteocytes and osteiod?
A

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.

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3
Q
  • What is the role of osteocytes and what system is this done by?
A

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

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4
Q

osteocytes regulate bone remodelling in response to mechanical and endocrine stimuli. Which factors favour bone formation and which factors favour bone reabsorption?

A

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

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5
Q

what is RANK, RANK ligad and OPG?

A
  • 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
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6
Q

what is the role of sclerostin in bone formation?

A

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.

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7
Q

what is the difference between Osteoporosis and osteomalacia

A

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.

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8
Q

what is the role of parathyroid hormone and Vitamin D in bones?

A
  • Increases Ca absorption from gut

* Synergistic effects with PTH on bone

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9
Q

what is the role of calcitonin in bones?

A
  • Negative feedback regulation of serum Ca
  • Released in response to rises in Ca
  • Inhibits osteoclast function
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10
Q

what are the actions of oestrogen on bones?

A
  • 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
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11
Q

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

A

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

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12
Q

what are some of the Pathophysiologies of frailty

A
  • 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
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13
Q

Sarcopaenia is a key component of frailty syndrome , what is it?

A

Sarcopeniais the degenerative loss of skeletal muscle mass quality, and strength associated with ageing.

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14
Q

explain the link between frailty and chronic inflammation

A
  • 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.
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15
Q

How is frailty diagnosed?

A

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

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16
Q

what is presbyesophagus and how is it managed?

A

Presbyesophagus is a term used to describe an abnormal shape of the swallowing tube (esophagus) that occurs in some individuals.
Problems with swallowing and esophageal dysmotility with older age

increase dietary fibre, adequate fluid intake, maitain mobilty, regular toileting, assess toileting condition

17
Q

explain the use of stimulant such as bisacodyl/senna to treat constipation

A
stimulation of nerves that control the muscles lining the digestive tract.
Senna is in a class of medications called stimulant laxatives. It works by increasing activity of the intestines to cause a bowel movement.
18
Q

what are symptoms of ageing skin

A

-decreased sebum production/ risk of dehydration- dry skin
-epidermal thinning
dermal thinning –> reduced ability to thermoregulate
reduced ability to casodilate in the capillary bed–> prone to heat retention
-prone to hyper/hypothermia
-loss of melanocytes so less protection from sun/paler
wrinkling and sagging of skin
-grey hair (Achromotrchia)
reduced syntethis of Vit D and melanin. Vit D essential for bone health so increases fracture risk.

19
Q

why does ageing skin cause pain?

A

dermal thinning –> reduction in nerve endings –> decreased sensation.

Neuropathic pain increases.

20
Q

pressure injury vs moisture lesion.

A

pressure- evidence of pressure or friction, usually over a bone distinct edges.

moisture lesion- skin moist/ history of incontinence, not over bone, edges may be difficult to determine

21
Q

what are some systemic causes of itchy skin?

A

renal faliure- build up of urea and waste materials

Liver: cholestatic- build up og bilirubin

22
Q

what is vasculitis and lymphedema ?

A

Vasculitis is an autoimmune disease that causes inflammation and narrowing of blood vessels

Lymphoedema is caused by a problem with the lymphatic system, a network of vessels and glands spread throughout the body. The main functions of the lymphatic system are helping fight infection and draining excess fluid from tissues.

23
Q

what is the role of parathyroid hormone?

A
  • Secreted by the parathyroid glands when blood calcium levels are low. 2nd - Stimulates osteoclast activity (resorption of bone occurs), which releases calcium into the blood. 3rd - Causes kidney tubules reabsorb calcium back into the blood.
24
Q

what are some endocrine causes of osteoperiosis?

A
  • Hypogonadism – notably any cause of oestrogen deficiency
  • Excess glucocorticoids – endogenous or exogenous (cortisol stress hormone so reduces bone formation)
  • Hyperparathyroidism
  • Hyperthyroidism
25
Q
  • How to diagnose osteoporosis?
A

a measurement of bone mineral density (BMD) and Dual-energy X-ray will give a t score.
Normal: -1 or above
Osteopenia: between -1 and -2.5
Osteoporosis: -2.5 or lower
Severe osteoporosis: -2.5 or lower and presence of at least one fragility fracture.

26
Q
  • What are some treatments for osteoporosis?
A
  • Ensure adequate calcium and vit D intake, appropriate exercise
  • Oestrogen – effects well established but safety of long term treatment has been questioned
  • Bisphosphonates – inhibit function of osteoclasts: risedronate, alendronate
  • PTH analogues
  • Denosumab – human monoclonal antibody against RANK ligand (since 2010)
  • Romosozumab – human MAB against sclerostin (since 2020)- causes acceleration on bone formation in response.

Guidelines for HRT modified
• Short-term therapy (3-5 years) for treating vasomotor symptoms
• Lowest effective dose to be used
• Long term use not recommended

27
Q

what are some intrinsic reasons that leads to falls.

A
  • Sacropenia
  • posture
  • brain atrophy
  • Bradykinesia (slowness of movement) can lead to falls
  • Hearing loss has a major affect on falling
  • Pupil becomes rigid and less elastic
  • Lens becomes opaque
  • Cataracts
  • Glaucoma
  • retinopathy
  • syncope (fainting/passing out)
  • osteopenia (loss of bone mass/weak bones)
28
Q

what is the difference between cataracts and glaucoma?

A

A cataract is a change in the lens of the eye; the result is cloudiness as light is prevented from entering the eye properly.

Glaucoma is a condition where a buildup of pressure in the eye causes damage to the optic nerve which is the vital link of the eye to the brain which processes visual information.

29
Q

what are some medications that are known to cause falls

A

Benzodiazepines are a type of medication known as tranquilizer. Familiar names include diazepam and temazepam

Hypnotics cause drowsiness. Zopiclone

Opiates can cause delirium.

Diuretics known to cause falls (diuretics increase the amount of water and salt expelled in urine)

sedating antidepressants
anti-epileptics 
alpha-blockers 
Beta blockers 
ACE inhibitors 
Sedating antihistamines.
30
Q

what is bradykinesia

A

Bradykinesia means slowness of movement and is one of the cardinal manifestations of Parkinson’s disease. Weakness, tremor and rigidity may contribute to but do not fully explain bradykinesia.

31
Q

what is the difference between an intracapsular and extracapsular hip fracture

A

Intracapsular
–Neck of femur
•Extracapsular
–Trochanteric (between femoral head and trochanters)
–Sub-trochanteric (bellow the lesser trochanter)
Search image online.

32
Q

what are some natural changes in gait as we age?

A

Reduced stride length•Reduced gait speed•Reduced hip flexion & extension•Wide based gait

33
Q

what is the initial management for hip fractures?

A
  • History–Trauma/Pain–History of or risk factors for osteoporosis
  • Examination–Shortened and externally rotated leg–Pain on movement–Inability to weight bear