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Semester 4 > Ageing, Impairment & Disability (AID) > Flashcards

Ageing, Impairment & Disability (AID) Flashcards

1
Q

What happens when you square the rectangle of survival?

A
  • Fall in infant mortality, higher living standards, better public health, better sanitation + better diet.
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2
Q

Chronically disabling diseases that have steep relationship to age?

A

Stroke, AD, Parkinsons, Osteoarthritis.

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3
Q

what happens in the Ageing process?

A
  • Impairment of function, which means there is a loss of adaptive responses to stress = growing risk of age related disease.
  • There are no symptoms of ageing - no pain and nausea etc.
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4
Q

What is frailty?

A
  • Physiological syndrome = decreased reserve and less resistance to stressors because of decline across lots of physiological systems. Causes vulnerability to adverse outcomes
  • Physical frailty is the combination of weight loss, fatigue, impaired grip strength, diminished physical activity or slow gait.
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5
Q

what are the differences in Ageing vs. disease

A
  • Disease needs identifying = can respond to treatment but ageing is not reversible. But ageing can be compensate able, so should not put all changes down to age.
  • Delaying onset of disabling disease to later ages when intrinsic ageing has raised fatality by reducing adaptability the average duration of disability before death is shorter = spend longer time living and shorter time dying.
  • Older you are when you become disabled = shorter dependency time before death. Disability in later life = postponement of age onset –> prevents suffering.
    > Universal, Intrinsic, Progressive, Deleterious, Individual, Intrinsic or extrinsic
    > Progressive but may be halted or reversed
    > Deleterious but may be arrested or cured
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6
Q

What are Strehlers concepts for a true ageing process

A
  • (ST)UPID
    Universal, Progressive, Intrinsic, Deleterious
  • Need all 4 to be a proper ageing process.
    Universal - identifiable in all members of species, affects people to different extent - e.g. collagen cross links and loss of calcium from the bones.

Progressive - changes progress with time like hair getting grey and losing muscle power.

Intrinsic - restricted to changes of endogenous origin. Skin in axilla, hair loss

Deleterious - eventually harmful to organism like loss of visual acuity + hearing

Health promotion, illness prevention, use technologies and find new technologies to postpone disability in old age.

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7
Q

What are the 3 theories of why we age?

A
  1. “Wear + tear”
  2. Adaptive evolutionary
  3. Non adaptive evolutionary
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8
Q

What are the 3 theories of why we age? - “Wear + tear”

A
  • Organism is a machine that wears out - like elephants teeth/weddell seal.
    • Not all animals age (e.g. Sea Anemone) - they have the ability to repair, e.g. germ line. We can repair whole organs e.g. Salamanders.
    • Therefore cannot be the whole answer
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9
Q

What are the 3 theories of why we age? - Adaptive evolutionary

A
  • Evolution + natural selection (Darwin Principles). Ageing can be selectively advantageous to species - prevents elderly and worn out animals competing
    • Advantage is to the population and not individual and is rarely seen in natural populations. B/c of circular arrangement, old and worn out ones cannot compete.
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10
Q

What are the 3 theories of why we age? - Non adaptive evolutionary

A

• There are 2 theories within this: mutation accumulation and antagonistic pleiotrophic genes + disposable soma theory

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11
Q

What is MUTATION ACCOMODATION

Within the non-adaptive evolutionary theory?

A
  • Less natural selection powers with age and the genes that are early expressed effect most of the population
  • The genes that get expressed after reproduction = lost from evolutionary control
  • Ageing is because of miscellaneous collection of late acting, deleterious genes

But there is no experimental support.

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12
Q

ANTAGONISTIC PLEIOTROPHIC GENES

Within the non adaptive evolutionary theory for ageing

A

There is an early good effect which is retained, and a bad late effect which contributes to ageing. Drosophilia studies support this.

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13
Q

The drosophilia experiments that support the non adaptive evolutionary theory for ageing within the antagonistic pleiotrophic genes - describe how?

A
  • AA (abnormal abdomen) allele greatly increases early fecundity and pleiotrophically reduces longevity.

If breeding is prevented until later in life over 15 generations then lifespan is extended by a third. Short winged flying is reduced.

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14
Q

Describe the disposable soma theory?

A
  • Development of non adaptive evolutionary views, this theory suggests that organisms are a machine that transfer free energy into progeny.
  • Success is to ensure that genes survive in the most efficient way
  • Disposable = produced with limited lifespan.
  • The soma is not of a germ line
  • Amount of energy that is used on up possibilities depends on ecological niche occupied by that organisms, which results in the species specific longevity. For some, fertility is priority. Others need to maintain soma for longer time period.
  • Entropy increases [via 2nd law of thermodynamics] - i.e. we age and decay, resist this with defensive and repair processes. These protective mechanisms eventually fail. The rate of ageing is determined by investment of self-maintenance.
  • = we are programmed to survive, not to age.
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15
Q

Processes through which we age?

A
  1. System level theories
  2. Cellular + molecular level theories
  3. Genetic theories
  4. Genomic stability
    • Theories are based on total body systems
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16
Q

Neuroendocrine theory of ageing?

A
  • There is a functional fall in neurones + associated hormones is central to ageing process and hypothalamic, pituitary and adrenal axis controls growth and development - so potentially ageing.
  • Decreased pulsatile GH + GnRH in ageing rats
  • Hypothesectomy + hormone replacement increases lifespan
  • DECO / death hormone is proposed but never found.
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17
Q

Describe cellular + molecular theories of ageing

• Wear + tear
A

“Wear + tear, and rate of living”

- Some rates of ageing look like wear and tear. Higher basal metabolic rate and shorter lifespan. Accumulation of damage might be important.
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18
Q

Cellular + molecular theories of ageing

• X link formation

A

Biological molecules develop cross linkage / bonds over time - changes physical/chemical properties. Collagen cross links.

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19
Q

describe heat shock proteins involved in ageing?

A
  • Produced @ time of cell stress. Disassemble damaged proteins and transport in new. Reduced production with age. Decreased ability to cope with stress = ageing.
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20
Q

What is the hayflick phenomena involved in ageing?

A
  • The fibroblasts that are grown in culture do certain # of divisions and then stop, and there is more divisions from a younger source. This is repeated in other cell types, we have biological clock.
  • HeLa cell line from Ca breast unlimited division.
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21
Q

Ageing genetic theories: Geronto genes, longevity assurance genes

A
  • Genes are important - twin studies, long lived families, species specific longevity.
  • Genes in drosophilia, yeast and nematodes have been seen that can shorten and lengthen life.

There can be a mutation in nematode that doubles 3/52 lifespan by increasing superoxide dismutase.

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22
Q

What can a mutation in nematode do in ageing?

A
  • Doubles 3/52 lifespan by increasing superoxide dismutase.
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23
Q

Characteristic of telomerase

A
  • Chromosome tail = repeated short DNA base sequence
  • Stabilise chromosome during cell division, gets shorter with division.
  • There is a critical length where divisions can no longer occur - which explains Hayflick phenomena. In germ cells + tumour cells telomerase is produced.
  • Germ and tumour cells make telomerase.
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24
Q

characteristics of Mice + telomerase?

A
  • Telomerase activity can change due to changes in comprehensive activity and telomere length in men, with biopsy proven low - risk prostate cancer
    • Shown by 10 subjects + 25 age matched controlled. Comprehensive lifestyle changes like diet and activity can alter.
    • Findings = telomere length increased from the base level in lifestyle intervention group but fell in control group!
    • Telomerase activity fell more in control group than in the lifestyle group
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25
Q

What can telomerase length regulate?

A
  • Can regulate ISG 15 expression in human cells
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26
Q

Genomic stability in ageing: error catastrophe

A
  • Errors in transcription + translation = weird protein production, can be fixed by replacing protein. If the protein is important in DNA repair / protein synthesis might lead to a cascade and then cell death.
  • Accumulation of such errors = ageing.
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27
Q

Somatic mutation + DNA repair - what occurs?

A
  • Based on irradiation, shortens life of mice - somatic mutation is now considered not as important because the occurrence rate is too low and DNA repair is sufficient.
  • However repair might fail in combo with other toxic agents, like UV and O2 radicals
  • DNA repair is more efficient in humans than in mice + more efficient in germ cells! Declines with ageing, which is more seen in cancer
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28
Q

What is the free radical theory of ageing?

A
  • Theory suggests that highly reactive chemical compounds come from enzymatic and non enzymatic reactions, which damage cellular DNA
  • Lots of enzymes like super oxide dismutase, catalase, glutathione peroxidase + vitamin E, C, and carotene protect cells - this protection reduces with age.
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29
Q

Describe the mitochondrial theory of ageing?

A
  • Ageing due to mitochondrial DNA damage and there is high exposure to O2 radicals - no protein coat to mitochondrial DNA. There is damage + mutation that increase with age. Genetic mitochondrial dysfunction syndromes mimic ageing.
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30
Q

Cell senescence characteristics?

A
  • Senescent cells # rise with age + are at site of age related pathologies like OA and pancreatic dysfunction.
  • Neurogenesis, haemopoesis, and pancreatic function decreases associated with p16 dependent senescence
  • Altered gene expression, and upregulated of genes that control enzymes that degrade ECM, inflammatory cytokines and growth factor
  • Disrupt normal tissue structure and function and stimulate the growth of premalignant cells.
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31
Q

Ageing changes - describe what happens

A
  • Due to many changes, accumulation of DNA damage = central.
  • The energy that is put into DNA repair and protection determines ageing rate.
  • Within genetic specific genetic makeup seems to influence rate of ageing via ability to resist DNA damage and external factors can influence ageing rate.
  • Calorie restriction can increase lifespan - also causes delayed puberty and increased infection in death prepuberty: okinawa diet.
  • Moderate exercise can have + effect

Overcrowding has - effect

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32
Q

What are the functions of parathyroid hormone on bone?

A
  • Stimulates bone resorption
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33
Q

What are the functions of parathyroid hormone on kidney?

A
  • Increases calcium absorption
  • Decreases phosphate, HCO3-, and Na+ reabsorption
  • 1alpha hydroxylase enzyme
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34
Q

What is the action of vitamin D in calcium homeostasis?

A
  • Increases ca2+ absorption in the gut
  • This process needs CaBPs - synthesis is stimulated by vitamin D
  • Synergises with PTH on bone
  • Inhibits PTH synthesis
  • Inhibits 1alpha hydroxylase
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35
Q

describe bones cells involved in tissue structure - osteoBLASTS

A
  • Bone forming cells
  • Secrete organic matric (osteoid)
  • Bone mineralisation
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36
Q

describe bones cells involved in tissue structure - osteocytes

A
  • May sense mechanical stresses and physiological conditions
  • Signal to other cells
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37
Q

describe bones cells involved in tissue structure - osteoclasts

A
  • Bone digesting cells, “diggers”

- Break down bone matrix releasing Ca and Pi into circulation

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38
Q

Describe the overview of bone remodelling

A
  • Continuous cycle of resorption and formation of new bone

Balance between osteoblast and osteoclast activity

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39
Q

Describe the induction of osteoclast differentiation by RANK ligand + define RANK/L and OPG

A
  • Osteoblast stimulates the differentiation of osteoclasts by the production of RANK ligand
  • This activates the RANK receptor on the osteoblast precursor
  • activation of nuclear kappa beta stimulates gene transcription and differentiation of osteoclasts
  • OPG binding to RANK inhibits differentiation
    RANK – Receptor Activator of Nuclear kappa beta.
    RANKL – RANK ligand
    OPG - osteoprotogenin
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40
Q

What is osteoporosis

A
  • Loss of bone mass
41
Q

endocrine causes of osteoporosis?

A
  • Hypogonadism : notably the cause of any oestrogen deficiency
  • Glucocorticoid XS, endogenous or exogenous
  • Hyperthyroidism, hyperparaythyroidism
  • Diabetes mellitus Type 1 (osteopenia)
42
Q

Haemotopoietic disease causes of osteoporosis?

A
  • Leukaemia

Sickle cell disease

43
Q

Drug inducedcauses of osteoporosis? (examples)

A
  • Heparin

- Anticonvulsants

44
Q

What is osteomalacia?

A
  • Loss of bone mineralisation
45
Q

How would you measure bone mineral density (BMD)

A

DEXA, DXA

T score

Z score

46
Q

What are the treatments for osteoporosis

A 
ERT/ HRT
Tibolone 
Anabolic steroids 
Selective estrogen receptor modulators (SERMs)
Biphosphonates 
Denosumab
47
Q

Adrenal androgens characteristics

A
  • Are the only source of female sex hormones after menopause - peripheral conversion to oestrogen
48
Q

Clinical signs of menopause

A
  • Vasomotor symptoms, hot flushes

- Later = accelerated bone loss, osteoporosis

49
Q

Hormone replacement therapy - progestogens

A
  • Short term therapy, and the lowest effective dose should be used. May be most effective if started closer to menopause.
Norethisterone
Medroxyprogesterone
Levonorgestral
Micronized cyproterone acetate
Dihydrogesterone
Drosperidone
50
Q

Function of the brain?

A
  • Computer that gets info, interprets it and makes a decision + controls breathing, BP maintenance, releasing hormones.
Frontal = Executive behaviour, impulsivity, emotions
Parietal = Sensory processing and reading + writing 
Temporal = Combination of auditory / visual information and memory
Occipital	= Visual processing
51
Q

Physical changes in the brain during ageing?

A
  • Atrophy, ventriculomegaly, neurone loss, increased density of NFTs, oxidative stress and increased inflammation, reduced cerebral blood flow.
52
Q

Brain Atrophy characteristics?

A
  • Decrease in the brain volume, and there is regional volume loss - especially in the frontal + temporal lobes
  • Grey matter falls once we get to adulthood
  • White matter increases until 40y/o, then declines. White matter loss is greater than grey matter loss.
53
Q

Characteristics of neurone loss?

A
  • CBM and ccx. Hypothalamus, pons, medulla are well preserved. Lose 10% of SN per decade. Not actually neuronal loss but there are changes in morphology that happen, and there is a reduction in communication.
54
Q

It is false that the brain does not make new neurones - why?

A

Continued production of neurones, but the losses > gains.

55
Q

characteristics of NFTS? (Neurofibrillary tangles)

A
  • Neurofibrillary tangles
  • Is associated with AD but also part of ageing and location = relative difference.
  • Normal ageing the number per cell body is low and tend to be confined to olfactory nucleus - parahippocampal gyrus and amygdala. With ageing there is an increase in density of tangles but there is no change in location.
56
Q

Describe process of oxidative stress

A
  • Accumulation of DNA lipid and protein by free radicals = functional decrease of the aged brain. Linked to inflammatory changes in microvascular changes. Brain is really sensitive to oxidative stress.
57
Q

What happens to cerebral blood flow of the brain?

A
  • Reduced by 5-20%, narrow arteries, fluctuant BP, homeostasis.
58
Q

Chemical effects in the brain - Serotonin

A
  • Depression and changes in circadian rhythm
59
Q

Chemical effects in the brain - Acetylcholine

A

Cognitive impairment

60
Q

Chemical effects in the brain -

Dopamine

A
  • Reduced arm swing and increased rigidity
61
Q

what happens to Serotonin, Acetylcholine, Dopamine as we age?

A
  • Fall in availability and production of all

- Largely due to reduction in synthesis, binding sites and # of receptors

62
Q

Neurophysiological effects on memory

A
  • Medial temporal lobe functions affected b/c of vulnerability to age related change, + there are procedural, primary and semantic memory are well preserved.
  • Episodic & working memory + executive function are not affected
  • Problem solving = steady decline.
  • Sematic memory is knowing that there are 10mm in 1cm (facts) and episodic memory is 1st day at school (memories).
63
Q

Characteristics of the Blood Brain Barrier?

A
  • Altered transport of nutrients, metabolites and toxins. Increased permeability. Reduced transport of glucose, proteins and hormones. More susceptible to hypoglycaemia.
  • Therefore hard to learn new things and get information, slower processing speed and problem solving gets worse, plus less able to reason unfamiliar things. Attending to and manipulate own environment and can be more difficult.
  • Starts to decline after the age of 30.
64
Q

When is there increased incidence of disease

A
  • Dementia, delirium, stroke, PD, vascular pathology.
65
Q

Parkinsons Disease characteristics

A

Neurodegenerative disease, death of cells that produce dopamine, in the Substantia Nigra. Gives tremor, rigidity, bradykinesia. 2nd commonest neurodegenerative disorder in AD. Some people are more predisposed - some people need dopamine more than others.

66
Q

What is cognitive reserve?

A
  • Brains ability to operate effectively even when some of the function is disrupted + amount of damage that brain can sustain before changes in cognition are evident.
  • Cognitive reserve variability is thought to be multifactorial and due to differences in genetics, education, occupation, lifestyle, leisure activities or other life experiences.
67
Q

Describe trigger delayed ageing

A

ducation, exercise, intellectual engagement, maintaining social networks, good diet.
- Brain can get sensitive to insults, depending on the ageing process + insult, can have different manifestations. Certain areas are vulnerable.

68
Q

What is delirium?

A
  • Acute confusional state
  • Common clinical syndrome is characterised by:
    • Disturbed consciousness
    • Cognitive function / perception
    ○ Has acute onset and fluctuating course.
  • It is hyperactive, hypoactive or mixed - hypoactive is the most common type
  • Increased risk over 65
  • Fluctuations / changes in cognitive function, perception, physical function and social behaviour.
    always acute onset, or fluctuating course + inattention plus ONE OF disorganised thinking or altered level of conciousness.
69
Q

What are the causes of delirium?

A
  • Infection, urinary retention, constipation, pain, cardio + resp, metabolic reasons, neuro, medications, drug and alcohol withdrawal, surgery and general anaesthetics, environmental factors like sleep deprivation/ immobility.
70
Q

What are characteristics of ALZ dementia?

A
  • Commonest cause of dementia - chronic neurodegenerative disorder.
  • Multiple hypotheses for cause: genetic, reduction in making Ach, amyloid deposits, Tau protein pairing to form NFTs.
  • Loss of neurones + synapses and atrophy espesh temporal + parietal lobes
  • Amyloid plauques and NFTs especially in temporal lobe
  • Can be treated with Achesterase inhibitors - Rivastigmine, Galantamine, Donepezil
71
Q

Give examples of the treatment of ALZ dementia with - Achesterase inhibitors

A

• Rivastigmine, Galantamine, Donepezil

72
Q

Give examples of the treatment of ALZ dementia with - NMDA receptor antagonists

A

• Memantine

73
Q

Bone types

A

Ø Cortical compact bone

Ø Trabecular bone (spongy cancellous) bone

74
Q

Describe the cellular structure of bone

A
  • OsteoCLASTS are derived from Hematopoietic stem cells
  • OsteoBLASTS are derived from Mesenchymal stem cells
    ○ Blast = makes everything a mess
  • Then the mature bone cells will sit as osteocytes
75
Q

Describe the characteristics of osteoblasts

A
  • Differentiate from mesenchymal stem cells
  • Bone forming cells
    • Lay down organic bone matrix (osteoid)
    • Promote mineralisation of the osteoid
  • Life cycle determined by control of differentiation + apoptosis
76
Q

What are the characteristics of osteoclasts

A
  • They are derived from haemotopoetic stem cells
  • Involved in the resorption of bone
    1. Secrete ACID, to dissolve + release the mineral content of the bone
    2. Enzymes release to degrade the organic matrix
  • Life cycle = determined by the control of differentiation & apoptosis
77
Q

Characteristics of osteocytes

A
  • Terminally differentiated, post mitotic osteoblasts
    • Entomed within the lacunae in the bone matrix
    • Communicate with each other + bone surface
    ○ Via cellular processes (dendrite) which run along canaliculi
    • Lacunar canalicular network
  • Might live for decades
78
Q

Describe the lacunar-canalicular network

A
  • Give the bone a more porous structure
79
Q

Describe the function of osteocytes

A
  • They regulate bone remodelling, in response to mechanical and endocrine stimuli
  • Function as endocrine cells
80
Q

Bone cellular structure

A
  • OsteoCLASTS are derived from Hematopoietic stem cells
  • OsteoBLASTS are derived from Mesenchymal stem cells
    ○ Blast = makes everything a mess
  • Loss/ gain of bone density is tipped when there are alterations in the numbers of osteoblasts, and osteoclasts (diggers)
81
Q

Describe the control of remodelling

- Factors that favour RESORPTION

A

Ø Unloading
• Bed rest, zero gravity etc.
Ø Anything that removes the mechanical loading on the bone - moves away from formation and decreases bone mass

82
Q

Describe the control of remodelling

- Factors that favour FORMATION

A

Ø Load bearing exercise

83
Q

Describe how the bone can act as a metabolic organ

A
  • Bone turnover serves homeostasis of serum: calcium, phosphate. This is in conjunction with:
    • Parathyroid hormone
    • Vitamin D (1,25 Di Hydroxy D3)
    • Calcitonin
  • In the short term, turnover of bone serves calcium homeostasis
84
Q

Describe the actions of PTH

A
  • PTH = maintains tight (negative feedback).
  • There is control of serum Ca, in the range of 2.2-2.6mmol per litre
  • PTH is released in response, to a fall in calcium
  • Stimulates bone remodelling (both anabolic and catabolic effects)
  • Stimulates the conversion of active hormonal vitamin D in the kidney
    • Stimulates 1 alpha hydroxylase
  • Increases Ca reabsorption in the kidney

Ø Major function is to regulate plasma calcium
Ø Also important role in bone formation & prevents osteoblast + osteocyte apoptosis

85
Q

More details on the action of PTH

A
  • Can function in short term control of calcium homeostasis, via osteoclastic activation
  • Effects on the bone are more complex; because it stimulates remodelling
  • Has anabolic and catabolic effects
  • PTH analogues can be effective as drugs, in order to treat diseases that involve bone loss (like osteoporosis)
  • PTH releases calcium into the circulation, this shows that it has catabolic effect, because it affects osteoclastic activity
  • Permanently raised = in treatment, small levels of analogues will actually increase bone mass
    • Not sure of the full mechanism - but it does have anabolic and catabolic effects
86
Q

What are the actions of vitamin D

A
  • Increases Ca absorption from the gut
  • Promotes differentiation of osteoclast and osteoblast lineages
  • Inhibits PTH release
  • Inhibits 1alpha hydroxylase
87
Q

Describe the actions of calcitonin

A
  • Negative feedback regulation of serum Ca
    Ø Released in response to increases of calcium
    Ø Importance in human Ca homeostasis is doubtful
    ○ e.g. if you were to have a thyroidectomy, you will also lose calcitonin (which is secreted by the C cells of the thyroid glands)
    ○ Receptors for calcitonin = present and it will have actions when given, directly inhibits osteoclast functions
  • Inhibits osteoclast function
88
Q

What are the actions of oestrogen

A
  • Regulates the life cycle, of osteoblasts and osteoclasts
    • OsteoCLASTS = shorten and promote apoptosis
    • OsteoBLASTS = lengthen (protect from apoptosis)
  • Indirectly inhibit osteoclast differentiation
  • Might be necessary for new bone formation, in response to mechanical stress
89
Q

Describe the cellular/molecular signalling in remodelling

A
  • Complex auto/para/endocrine network involving multiple cell types
90
Q

Describe the induction of osteoclast differentiation by RANK ligand.

A

Ø RANK (Receptor Activator of Nuclear Factor Kappa B)
Ø Surface receptor on Pre-osteoclasts
○ Stimulates osteoclast differentiation
Ø RANK-Ligand, produced by pre-osteoblasts, osteoblasts, and osteocytes
Ø Binds to RANK and stimulates osteoclast differentiation

91
Q

What is the role of OPG (osteoprotogenin)

A
  • This is a decoy receptor
  • Is produced by the osteocytes
  • Binds to RANK-Ligand
  • Therefore preventing the activation of RANK; because it blocks RANKL.
92
Q

Osteocyte regulation of bone remodelling

A
  • Osteocytes express RANKL + macrophage colony stimulating factor (M-CSF) to promote
    • Uses OPG, and NO to inhibit osteoclast formation and activity
    • Osteocytes also regulate bone formation, via the secretion of modulators of the WNT signalling pathway
      ○ PGE2, NO & ATP act, to activate WNT signalling
      ○ Sclerostin, DKK1, and SFRP1 all inhibit WNT signalling and subsequnt osteoblast activity
    • Maintenance of this balance between resorption and formation by the osteocyte is essential for bone homeostasis
93
Q

Describe the metabolic bone disease: osteoporosis

A
  • Osteoporosis is the loss of bone mass
    ○ + thinning of the bone, eating away at the trabecular bone
    ○ This is due to endocrine reasons
    ○ Malignancy = any cancer than metastasises to the bone
    ○ Drug induced
    ○ Renal disease
    ○ Nutritional
  • Osteomalacia = the loss of bone mineralisation, leading to softening of the bone
94
Q

What are the endocrine causes of osteoporosis

A
  • Hypogonadism = notably any cause of oestrogen deficiency
  • Excess glucocorticoids- endogenous or exogenous
    • e.g. cortisol (via Cushings or Glucocorticoid Treatment as a side effect)
    • Cortisol = has a catabolic effect on bone loss
  • Hyperparathyroidism
  • Hyperthyroidism
95
Q

Describe how you would diagnose osteoporosis

A

T-Score
Ø Unit of standard deviation
Ø Look @ how many SDs below average for young adult @ peak bone density

Z-Score
Ø Matched to age, and or group

96
Q

What are the clinical manifestations of the menopause

A
  • Vasomotor symptoms (hot flushes)

- Later - : there is accelerated bone loss, osteoporosis

97
Q

Describe the treatments for osteoporosis - Bisphosphonates

A

Ø Inhibits the function of osteoCLASTS
Ø Resdronate, (alendronate = most common)
Ø These are the first line treatments

98
Q

Describe the treatments for osteoporosis - Denosumab

A

Ø Antibody against RANK ligand

Ø This is human monoclonal antibody against RANK ligand

Semester 4 (10 decks)

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