Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Disease, diagnostics and therapeutics > Frailty > Flashcards

Frailty Flashcards

1
Q

frailty

A

‘multiple physiological systems losing reserves”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

frailty

A
  • muscle, immunity, endocrine signalling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

frailty is

A

reversible and preventable and not inevitable in ageing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

frailty and hormones

A

endocrine changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

frailty and msucles

A

weakening of the muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

frailty and the brain

A

degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

sarcopenia

A

loss of muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cardiac muscle is striated and cardiomycoytes are connected via

A

intercalated discs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

not couple- but activated by the influx of calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cardiac muscle and ageing

A

heart tissue thickens and stiffens,increasing risk of cardiovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

smoot muscle

A

no sarcomeres- non striated

  • single nucleus int he centre of the cell
  • basal lamina surround cells containing extraceullualr proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

s.muscle is activate by

A

stretch, nervous hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how is s. muscle contraction different

A

NO TROPONIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gi and smooth muscle

A

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

- vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Gs and smooth muscle

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

example of Gq GPCR in smooth muscle

A

ADH V1 R and angiotensin II AT1R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

s. muscle and ageing

A

signify decrease in s.muscle function with increased age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

skeletal muscle fibres

A

behave as a single unit, multinucleate.

Surrounded by sarcoplasmic reticulum with invaginated T-tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

in skeletal muscle contraction..

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

as you get older skeletal muscle

A

decreases due to sarcopenia and we become weaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how many hallmarks of ageing are there

A

9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

there more hallmarks (aggregation)

A

the more accelerated ageing is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the 9 hallmarks of ageing

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

only cells expressing the enzyme telomerase can

A

make DNA at the end of telomerases

29
Q

cells which express telemorase

A

stem cells (can reproduce forever) and cancer cells

30
Q

everytime cells of through mitosis

A

telomeres shorten

31
Q

shortening of telomeres=

A

Hay flick limit

32
Q

Epigenetic alterations

A

histone modifications and DNA methylation change gene expression

33
Q

methylation =

A

turns off

34
Q

actetylation=

A

turns on

35
Q

loss of proteostasis

A

protein misfiling and aggregation e.g. parkinsons

36
Q

deregulated nutrient sensing

A

can cause less IGF- meaning less protein synthesis as you get older

37
Q

Mitochondrial dysfunction

A

ROS- apoptosis like excitotoxicity

38
Q

cellular sensence

A

increase the likelihood of disease of ageing

39
Q

senescent cells

A

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
Q

senescent cells make disease like

A

diabetes and liver failure more common

e.g. autoimmune diseases

41
Q

cure for ageing?

A

if we could kill off scene sent cells- e.g. mice will live 30% longer in better health

42
Q

stem cell exhaustion

A

decline in blood cells e.g. adaptive immune cells and reduced chemotactic motility of innate neutrophils

43
Q

how are neutrophils affected by ageing

A

reduced chemotactic motility of innate neutrophils

44
Q

myostatin

A

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
Q

when myostatin is bound to receptor

A

leads to pathways which breakdown muscle- decreasing muscle mass
- not sure if levels change in ageing, but definitely increased in obesity

46
Q

if myostatin gene is mutated or deleted

A

can increase muscle mass

47
Q

catabolic state

A

when proteins are being broken down- muscle mass decreases- sarcopenia

48
Q

as we get older and if on restricted diet IGF-1

A

decreases

49
Q

why does IGF-1 decrease

A

due to epigenetic switching off and deregulation of fiet

50
Q

reduced exercise and activity often occurs with age and this causes

A

atrophy of muscle

51
Q

which pathway is associated with inflammaging

A

NF-kB

52
Q

immunoscencence

A

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
Q

immunescence is a major contributing factor

A

to increased frequency of morbidity and mortality among the elderly

54
Q

Hemtopoietic stem cells and immunoscence

A

Reach senescence
Due to DNA damage
Oxidative stress increases over time to reduce cell cycle due to mitochondrial feedback

55
Q

macrophages and and immunoscenence

A
  • phagocytic ability decreases

- number decreases

56
Q

T-helper cell and and immunoscence

A

and immunoscence

57
Q

T killer cell and immunoscence

A

Thymus size decreases from birth
Number of T cell produced decreases
Cytotoxicity decreases

58
Q

B cell and immunoscence

A

Number decreases
Smaller pop. mean fewer immunoglobulins produced
Opsonisation by Ig decreases- less effective at drawing in T cells

59
Q

Natural killer cells and immunoscence

A

cytotoxicity decreases with age
They become less effective at killing pathogens
More susceptible to viral infections

60
Q

inflammaging

A

chronic inflammation

  • skin detrioates
  • joint ache
  • heart disease
  • cancer
  • arthritis
  • alzhemers
61
Q

inflammaging activates

A

innate immunity and macrophages ar eno longer able to turn off.
- pro-inflmamtory cytokines e.g. TNF-alpha= inflammaging

62
Q

causes of inflammaging

A
  • stress
  • oxidative stress
  • DNA damage
  • stem cell aaeing
63
Q

pathways associated with inflammaging

A
  • NF-kB
  • TOR- activates NF-kB
  • RAS0 activates pro-inflmmaotry cytokine production
64
Q

NF-kB

A

regulating ageing and inflammation

65
Q

TOR

A

regulates growth and proliferation of cells (always

Activating NF-kB)

66
Q

RAS

A

activation leads to pro-inflammatory cytokine production

Vascular inflammation and senescence

67
Q

which gene encodes myostatin

A

MST- member of TGF beta protein family

68
Q

individuals who have mutations in both copies of myostatin gene have

A

significantly more muscle mass and are stronger than normal

Disease, diagnostics and therapeutics (53 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions