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Disease, diagnostics and therapeutics > Frailty > Flashcards

Frailty Flashcards

1
Q

frailty

A

‘multiple physiological systems losing reserves”

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2
Q

frailty

A
  • muscle, immunity, endocrine signalling
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3
Q

frailty is

A

reversible and preventable and not inevitable in ageing

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4
Q

frailty and hormones

A

endocrine changes

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5
Q

frailty and msucles

A

weakening of the muscle

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6
Q

frailty and the brain

A

degeneration

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7
Q

sarcopenia

A

loss of muscle

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8
Q

cardiac muscle is striated and cardiomycoytes are connected via

A

intercalated discs

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9
Q

cardiac muscle contraction via

A

Gs

1) activation of adenylyl cyclase
2) increase in cAMP
3) increase in PKA
4) PKA phosphorylates calcium L type channels so they open causing an influx of calcium
5) calcium induced calcium release when calcium binds to calmodulin
6) Ca/Calmodulin complex binds to MLCK- contraction
6) MLCP removes phosphates- causing relaxation

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10
Q

In cardiac muscle contraction L-type Calcium channels and RyRs are

A

not couple- but activated by the influx of calcium

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11
Q

cardiac muscle and ageing

A

heart tissue thickens and stiffens,increasing risk of cardiovascular disease

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12
Q

smoot muscle

A

no sarcomeres- non striated

  • single nucleus int he centre of the cell
  • basal lamina surround cells containing extraceullualr proteins
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13
Q

s.muscle is activate by

A

stretch, nervous hormones

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14
Q

s. muscle contraction

A

via Gq

1) when activated Gq cause IP3 to be hydrolysed
2) hydrolysed to PIP2 and DAG
3) PIP2 causes the SR to release calcium, calcium binds to calmodulin and causes activation of MLCK- contraction
4) MLCP removes phosphate from MLC causing relaxation

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15
Q

how is s. muscle contraction different

A

NO TROPONIN

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16
Q

Gi and smooth muscle

A

e. g. A2contraction- due to less cAMP inhibiting MLCK

- vasoconstriction

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17
Q

Gs and smooth muscle

A

e. g B2 relaxation
- more cAMP
- increased inhibition of MLCK
- vasodilation

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18
Q

example of Gq GPCR in smooth muscle

A

ADH V1 R and angiotensin II AT1R

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19
Q

s. muscle and ageing

A

signify decrease in s.muscle function with increased age

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20
Q

skeletal muscle fibres

A

behave as a single unit, multinucleate.

Surrounded by sarcoplasmic reticulum with invaginated T-tubules

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21
Q

Skeletal muscle contraction

A

1) AP reaches sarcoma causing depolarisation
2) depolarisation is conducted down the T-tubules
3) depolarisation causes conformation change in the dihydropyridine receptors, which are mechanically coupled with RyRs
4) conformational of DHPR causes RyR to be activated and calcium to be released from the SR
5) calcium binds to troponin, which means myosin heads are now able to form cross bridges with actin - contraction

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22
Q

in skeletal muscle contraction..

A

contraction is maintained for as long as calcium is bound to troponin

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23
Q

as you get older skeletal muscle

A

decreases due to sarcopenia and we become weaker

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24
Q

sarcomeres and ageing

A
  • lost with raging
  • reduction in muscle fiber lengt due to a decree in sarcomere number
  • sarcomere spacing becomes disorganised
  • muscle nuclei become centralised along the muscle fibre
  • plasma membrane becomes less excitable
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25
how many hallmarks of ageing are there
9
26
there more hallmarks (aggregation)
the more accelerated ageing is
27
what are the 9 hallmarks of ageing
1) genomic instability 2) telomere attrition 3) epigenetic hanges 4) loss of proteostatis 5) deregulated nutrient sensing 6) mitochondrial dysfunction 7) cellular senescence 8) stem cell exhaustion 9) alter intracellular communication
28
only cells expressing the enzyme telomerase can
make DNA at the end of telomerases
29
cells which express telemorase
stem cells (can reproduce forever) and cancer cells
30
everytime cells of through mitosis
telomeres shorten
31
shortening of telomeres=
Hay flick limit
32
Epigenetic alterations
histone modifications and DNA methylation change gene expression
33
methylation =
turns off
34
actetylation=
turns on
35
loss of proteostasis
protein misfiling and aggregation e.g. parkinsons
36
deregulated nutrient sensing
can cause less IGF- meaning less protein synthesis as you get older
37
Mitochondrial dysfunction
ROS- apoptosis like excitotoxicity
38
cellular sensence
increase the likelihood of disease of ageing
39
senescent cells
stay around and don't die due to not producing much apoptotic proteins. These cells cause damage to tissue due to pro-inflammatory cytokines causing INFLAMMAGING
40
senescent cells make disease like
diabetes and liver failure more common e.g. autoimmune diseases
41
cure for ageing?
if we could kill off scene sent cells- e.g. mice will live 30% longer in better health
42
stem cell exhaustion
decline in blood cells e.g. adaptive immune cells and reduced chemotactic motility of innate neutrophils
43
how are neutrophils affected by ageing
reduced chemotactic motility of innate neutrophils
44
myostatin
Myostatin is a myokine, a protein produced and released by myocytes that acts on muscle cells' autocrine function to inhibit myogenesis: muscle cell growth and differentiation. In humans it is encoded by the MSTN gene.
45
when myostatin is bound to receptor
leads to pathways which breakdown muscle- decreasing muscle mass - not sure if levels change in ageing, but definitely increased in obesity
46
if myostatin gene is mutated or deleted
can increase muscle mass
47
catabolic state
when proteins are being broken down- muscle mass decreases- sarcopenia
48
as we get older and if on restricted diet IGF-1
decreases
49
why does IGF-1 decrease
due to epigenetic switching off and deregulation of fiet
50
reduced exercise and activity often occurs with age and this causes
atrophy of muscle
51
which pathway is associated with inflammaging
NF-kB
52
immunoscencence
the gradual deterioration of the immune system, brought on by ageing. refers to the hosts capacity to response to infection as well as the development of long term immune memory
53
immunescence is a major contributing factor
to increased frequency of morbidity and mortality among the elderly
54
Hemtopoietic stem cells and immunoscence
Reach senescence Due to DNA damage Oxidative stress increases over time to reduce cell cycle due to mitochondrial feedback
55
macrophages and and immunoscenence
- phagocytic ability decreases | - number decreases
56
T-helper cell and and immunoscence
and immunoscence
57
T killer cell and immunoscence
Thymus size decreases from birth Number of T cell produced decreases Cytotoxicity decreases
58
B cell and immunoscence
Number decreases Smaller pop. mean fewer immunoglobulins produced Opsonisation by Ig decreases- less effective at drawing in T cells
59
Natural killer cells and immunoscence
cytotoxicity decreases with age They become less effective at killing pathogens More susceptible to viral infections
60
inflammaging
chronic inflammation - skin detrioates - joint ache - heart disease - cancer - arthritis - alzhemers
61
inflammaging activates
innate immunity and macrophages ar eno longer able to turn off. - pro-inflmamtory cytokines e.g. TNF-alpha= inflammaging
62
causes of inflammaging
- stress - oxidative stress - DNA damage - stem cell aaeing
63
pathways associated with inflammaging
- NF-kB - TOR- activates NF-kB - RAS0 activates pro-inflmmaotry cytokine production
64
NF-kB
regulating ageing and inflammation
65
TOR
regulates growth and proliferation of cells (always | Activating NF-kB)
66
RAS
activation leads to pro-inflammatory cytokine production | Vascular inflammation and senescence
67
which gene encodes myostatin
MST- member of TGF beta protein family
68
individuals who have mutations in both copies of myostatin gene have
significantly more muscle mass and are stronger than normal

Disease, diagnostics and therapeutics (53 decks)

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