age-related deterioration
senescence
senescence occurs ( )
cell by cell
what body systems do senescence affect?
all of them
causes senescence: damaged cells are less ( )
robust
causes senescence:reactive oxygen species (oxidants) vs ( )
antioxidants (vitamins C and E)
causes senescence: telomeres and cell ( )
retirement
causes senescence:excessive ( )
apoptosis
causes senescence: genetic disorders of accelerated aging
progeria
progeria is usually a ( ) mutation…is it heriatable?
spontaneous point mutation; not heritable
what does progeria interfere with?
cells ability to reproduce (no new cells to replace old ones)
how common is progeria?
very rare; many varieties
progeria: few survive to what age?
15
progeria: cause of death is usually what?
atherosclerosis
how senescence affects skin
sunlight damage
how senescence affects musculoskeletal
osteoporosis, myoatrophy, osteoarthritis
how senescence affects CVS
limited max HR, output; hypertension
how senescence affects respiratory
decreased capacity; COPD
how senescence affects GI
liver slow to clear drugs, toxins; poor nutrition, constipation, dehydration
how senescence affects GU
low GFR, incontinence, vaginal dryness, erectile dysfunction
how senescence affects CNS
decline of cognitive power, reflexes; Alzheimer’s, Parkinson’s
how senescence affects Senses
deafness, loss of smell, dry eyes
what is the key of stress
perception
the stress response includes what 3 phases?
alarm, adaption, exhaustion
stress response phase: sympathetic NS, endocrine; fight or flight
alarm
stress response phase: perception; physical
adaptation
stress response phase: failed adaptation
exhaustion
stress exhaustion harms ( )
cells and systems
stress and cells/systems: common link
cortisol= impaired immune function= impaired glucose metabolism (diabetes) and immune surveillance (cancers)
physical stress
chronic inflammation (atherosclerosis accelerated aging, impaired DNA repair mechanism, oxidative stress)
mental stress: acute
terrorizing flashbacks, panic, withdrawal
mental stress: chronic
PTSD, longer version of acute
immobility: muskuloskeletal
atrophy, flexion contractures, osteopenia
immobility: skin
decubitis (pressure) ulcers
immobility: CVS
deep venous thrombosis
immobility: respiratory
hypoventilation, pneumonia
immobility: GI
contipation
sensation apart from origin
referred pain
pain is classified by ( )
duration and origin
pain classification: disappears with healing, associated with anxiety, tachycardia, tachypnea
acute
for pain to be classified as chronic, how long must pain be?
more than one month
pain classification: signal from pain receptors in injured site
nociceptive
pain classification: injury to or dysfunction of nervous system
neuropathic
options in pain treatment are largely ( )
pharmacologic
patients lack ( ) to say what pain is
verbal
chronic pain mechanism: injury heals, pain remains
sensitized transmission circuits
chronic pain mechanism: pain relief by antidepressants, anticonvulsants
variable cortical interpretation (perception)
chronic pain: ( ) involves nervous system damage or dysfunction
neuropathic pain
chronic pain pharacologic treatments:
analgesia, anethesia, anti-inflammaotory
mechanisms that may provoke chronic pain
1) chronic injury and altered perception (fibromyalgia)
2) accelerated cellular aging
3) increased oxidative stress
chronic pain: involves nervous system damage or dysfunction
neuropathic pain
neuropathic pain: relfex sympathetic dystrophy and causalgia
complex regional pain syndrome