Brainscape's Knowledge GenomeTM

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


See full index

DDT > 8 - frailty > Flashcards

8 - frailty Flashcards

1
Q

sarcopenia

A

loss of muscle mass, strength and quality

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

aging is a … process

A

heterogenous

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

how many hallmarks of aging

A

9

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

genomic instability

A

hallmark of aging
DNA damage accumulation
exogenous or endogenous cause
creates lesions

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

telomere attrition

A

shortening of telomeres

telomeres are required for normal cell divison

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

epigenetic alterations

A

changes in DNA methylation

changes in histone modification

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

loss of protestasis

A

proteins become unstable and unfolded

causes aggregation

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

deregulated nutrient sensing

A

caused by genetic polymorphisms

growth factors e.g. IGF-1
targets = FOXO/mTOR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

mitochondrial dysfunction

A

destabilisation of ETC

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

cellular senescence

A

stable arrest of cell cycle

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

stem cell exhaustion

A

types of stem cell:

  • haematopoietic
  • mesenchymal
  • satellite
  • intestinal epithelial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

altered intracellular communication

A

neuroendocrine dysfunction
inflammaging
immunosenescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

programmes theory of aging

A

deteriation is inevitable over time

  • programmed longevity
  • endocrine theory
  • immunological theory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

programmed longevity

A

sequential switching on and off of switches over time causes deteroiration

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

damage and error theory consists of 5 parts

A 
wear and tear
rate of living
cross-linking proteins
free radicals
somatic DNA damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

rate of living theory

A

greater metabolism = shorter life span

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

free radicals theory

A

cause oxidative damage to macromolecular cell components

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

what does ELISA stand for

A

enzyme-linked immunosoribent assay

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

what is ELISA

A

plate based assay technique

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

what does elisa used for

A

detecting and quantifying peptides, proteins, antibodies and hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

rt-pcr stands for

A

reverse transcriptase polymerase chain reaction

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

rt-pcr steps

A
  1. convert RNA population to cDNA by reverse transcription

2. amplify cDNA by PCR

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

why is rt-pcr useful

A

allows more detailed study of original RNA species even if they are expressed in low abundance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

uses of rt-pcr

A

detection of expressed genes
examination of transcript variants
generation of cDNA templates for cloning and sequencing

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

one step rt-pcr

A 
single tube
combines cDNA synthesis and PCR otgether
reduces variation 
reduces contamination 
quicker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

two step rt-pcr

A

cDNA synthesis and PCR in separate tubes and reaction s
used for detecting multiple genes in the same sample
can reach optimum reaction conditions
longer workflow
less contamination

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

how do you test for different genes in the same sample with rt-pcr

A

2 step method

make different specific primers for each time you run PCR

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

define senescence

A

loss of a cell’s power to divide and grow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

main mechanism of senescence

A

telomere shortening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

why do telomeres shorten

A

linear DNA is not completely replicated every mitosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

DNA damage response

A

when telomeres reach a critically short length

they become dysfunctional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

hayflick limit

A

when a cell has reached its maximum amount of times it can divide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

why are cancer and stem cells immortal

A

their DNA doesnt shorten
no hayflick limit
they express telomerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

telomerase

A

adds telomere back on when lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

effect of DNA damage/telomere malfunction

A

premature senescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

benefit of senescence

A

helps prevent tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

cons of senescence

A

causes ageing
age-releated diseases
prevents tissues reparing well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

accumulation of senescence

A

negatively affects tissue structure and fucntion leading to frailty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Senescence associated secretory phenotype

A

secreted factors by senescing cells

e..g proinflammatory cytokines, chemokines, proteases, growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

immunosenescence

A

gradual deterioration of the immune system with age

41
Q

immunosenescence cellular effects

A

defects in haematopoietic stem cells

defects in peripheral lymphocyte migration, maturation and function

42
Q

overall effects of immunosenescence

A

increased infection , cancer and autoimmune disease

43
Q

why does immunosenescence cause decreased adaptive immune resposne

A

causes decreased antigen presentation

44
Q

thymic involution

A

immunosenescence causes decrease in thymuc tissue mass

leads to loss of naive t cells

45
Q

inflammaging

A

chronic inflammation associated with age

chronic inflammatory cytokine production

46
Q

process of inflammaging

A

irritation causes cell membrane damage
causes arachidonic acid to be cut into leukotrienes and prostaglandins
inflammatory leukotrienes cause free radical damage

47
Q

effect of free radicals produced by inflammaging

A

cause elastase and collagenase to affect skin and destruct skin structure

48
Q

role of inflammaging in cancer

A

reduces immune response to new antigens

49
Q

direct ELISA

A

target antigen bound to bottom of well
complementary primary labelled antibody added
antibody binds to antigen
enzyme label catalyses colour change reaction

50
Q

advantages of direct elisa

A

cross-reactivity of secondary antibody eliminated

not max reactivity as antibody is labelled

51
Q

indirect elisa

A

antigen bound to bottom
primary antibody added and binds to antigen
well washed to remove any non-bound antibodies
secondary enzyme-linked antibody added
- complementary to constant region of primary antibdy
enzyme label causes colour chnage

52
Q

advantages of inirect elisa

A

maximum immuno-reactivity of primary antibody as it isnt labelled

53
Q

sandwich elisa

A 
antibody bound to bottom of well
target antigen added and binds
well washed - removes non-bound antigen
secondary enzyme-labelled antibody added
colour change measured
54
Q

advantages of sandwich elisa

A

allows concentration of unknown substances to be measured

most common one

55
Q

characteristics of apoptosis process

A

chromatin condensation
nuclear fragmentation
blebbing and cell shrinkage
release of apoptotic bodies

56
Q

extrinsic apoptosis pathway

A 
Fas binds to death receptor
transautophosphrylation of RTK
death inducing complex formed
activation of caspase-8
activation of effector caspases e.g. caspase-3
apoptosis
57
Q

intrinsic apoptosis pathway

A 
intracellular damage/ no growth factor 
Bad not phosphorylated
Bcl-2 inihibited 
mitochondrial dysfunction 
release of cytochrome-c into cytosol
caspase-9 activated
effector caspases activated - eg caspase-3
apoptosis
58
Q

Bad protein in presence of trophic factor

A

Bad gets phosphorylated
binds to Bcl-2
no apoptosis

59
Q

process of necrosis

A 
cell swells
chromatin digested
organelle membranes disrupted
cells lyse and spill contetns
hydrolytic enzymes damage neighbouring cells
inflammation
60
Q

cause of auto-phagy

A

response to cell starvation and stress or if organelles wear out
source of energy for cell

61
Q

autophagy in cellular homeostasis

A

digestion of intracellular components

degradation products transloacted to cytoplasm

62
Q

microautophagy

A

invagination of lysosomal membrane

sequesters proteins and degrades

63
Q

macroautophagy steps

A

isolation membrane
vesicle elongates to form phagophore
autophagosome formation - double membrane
LC3 allows binding to lysosome
autolysosome forms
contents broken down by acid proteases/hydrolytic enzymes

64
Q

defects in autophagy

A

prevent cells from clearing unwanted proteins/microbes

allow disease manifestation

65
Q

principal mechanism for protein catabolism

A

ubiquitin proteasome pathway

66
Q

role of E1-activating enzyme

A

binds to Ub
primes Ub
adds ATP

67
Q

role of E2-conjugating enzyme

A

binds to Ub and replaces E1

escorts Ub to E3 enzyme

68
Q

role of E3-ubiquitin ligase enzyme

A

acts as a platform fro E2-Ub complex to bind to targeted protein
Ub is then transferred to protein

69
Q

type I skeletal muscle fibres

A 
slow twitch fibres
red 
aerobic respiration 
slow-contracting
low myosin ATPase activity
70
Q

type IIa skeletal muscle fibres

A 
fast oxidative fibres
red
aerobic respiration 
fast-contracting
higher myosin ATPase activity
71
Q

type llb skeletal muscle fibres

A 
fast glycolytic fibres 
white 
fast-contracting
anaerobic respiration 
lower capactiy for ATP production 
sparser capillary network 
less sustainable
72
Q

what triggers contraction of cardiac muscle

A

calcium induced calcium release

triggers opening of ryanodine receptor

73
Q

characteristics of cardiac muscle

A

involuntary

striated - intercalated disks

74
Q

cardiomyocyte

A

heart muscle cell

75
Q

diseases of cardiac muscle

A

caused by restriction to blood supply
angina
myocardial infarction

76
Q

t-tubules in cardiac muscle

A

bigger/wider than skeletal muscle
transmit action potentials to cells core
regulate Ca2+ conc in excitation-contraction coupling

77
Q

angina

A

obstruction to coronary arteries
reduces blood flow to heart
heart cant contract properly
chest pain

78
Q

PI3/Akt pathway until PIP3 is activated

A

signal binds to RTK
receptor dimerisation and transautophosphorylation
PI3 recruited via SH2 domain
PIP2 converted to PIP3

79
Q

PI3/Akt pathway once PIP3 is activated

A

PIP3 recruits Akt and PDK-1 via their PH domains
PIP3 binds to Akt
Akt phosphorylated by MTORC2 and PDK-1
Akt downstream affects

80
Q

3 downstream effects of phosphorylated Akt

A

1 - activation of Rheb by inactivation of TSC2
MTORC1 activated - growth

2 - activation of AIP (apoptosis inhibiting) by inactivating Bad - cell survival

3 - inactivation of FOXO (T. factor) which prevents transcription of atrogenes in myofibres (prevents autophagy)

81
Q

3 overall effects of PIP2/Akt pahway

A

activation of MTORC1 - cell growth
inhibition of apoptosis - cell survival
inhibition of autophagy

82
Q

PI3-Kinase

A

converts PIP2 to PIP3

83
Q

mTOR

A

mammalian target of rapamycin

84
Q

mTOR involevd in

A

cell growth, proliferation

85
Q

regulation of mTOR

A

growth factors, insulin, glucose

86
Q

inactivated TSC2

A

activated Rheb

activated MTORC1

87
Q

mTOR pathway in presence of growth factor

A 
Akt causes inactivation of TSC2
activation of Rheb
(Rheb-GTP)
activae mTOR
cell growth
88
Q

mTOR in absence of growth factor

A 
TSC2 active
acts as a GAP to Rheb
Rheb-GDP (inactive)
inactive mTOR
no cell growth
89
Q

myostatin

A

protein produced and released by myocytes that inhibits myogenesis

90
Q

myogenesis

A

determines muscle fibre number in development and muscle size in adults

91
Q

increased myostatin

A

decreased muscle mass

92
Q

effect of myostatin on Akt

A

inhibits Akt
inhibition of protein synthesis
myofibirl degradation
muscle atrophy

93
Q

inhibition of myostatin as a therapuetic

A

for sarcopenia (prevent muscle wasting)

94
Q

IGF-1

A

insulin like growth factor
produced in liver
stimualted by growth hormone
binds to RTK

95
Q

IGF-1 pathway

A 
IGF-1 binds to RTK
receptor dimerisation and transautophosphorylation
activation of PI3-K via SH domain 
PIP2 to PIP3 
Akt recruited
mTOR pathway initiated 
protein synthesis etc
96
Q

effects of IGF-1

A

protein synthesis
inhibition of proteolysis
stimulates nutrient uptake

97
Q

IRS-1

A

signalling adaptor protein
has a PH domain
binds to RTKs

98
Q

IRS-1 pathway

A

ligand binds to RTKs
transautophosphorytion
IRS-1 binds via PH domain
recruits docking proteins bind via SH2 domains
e.g. grb2 and PI3-K
Activates downstream pathways e.g. MAPK and PI3-K/Akt

DDT (12 decks)

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