Powerpoint-Chap1 Flashcards
What are the main contributors to cellular aging
telomere shortening, environmental insults, DNA repair defects, Abnormal growth facto signaling
How is it hyposthesized that sirtuins reduce aging
insulin sensitization, decreasing free radicals and prevention of apoptosis
What to sirtuins require for action
NAD
What pharm agent induces Sirt1 activity
resveratrol
What is the first line of defense against cell injury
atrophy, hypertrophy, hyperplasia, metaplasia for ways of adaptation
inability of a cell to adapt leads to what
irreversible or reversible injury
Addition of growth factors and hormones can lead to what cell adaptations
hyperplasia and hypertrophy
decreased nutrients and stimulation can lead to what cell adaptations
atrophy
chronic irritation whether physical or chemical can lead to what cellular adaptation
metaplasia
actue transient hypoxic or injurious attacks lead to what type of cell injury
reversible. cell may swell or there are fatty changes
progressive and severe hypoxic or chemical attacks lead to what type of cell injury
irreversible
cell death by necrosis or apoptosis
metabolic alterations can lead to what type of cell response
intracellular accumulation, calcification
cumulative sublethal injury results in what type of cell response
cellular aging
having a cast causes what type of atrophy
decreased workload/disuse
what can cause denervation
disease or lack of use
what is worse, hypoxia or ischemia
ischemia
what is marasmus
really total malnutrition
breakdown fat really well still
what is cachexia
wasting away from diseases that cannot be reversed nutritionally
how does atrophy happen from endocrine system
loss of stimulation from those hormones
what is a pressure atrophy
presses on surrounding structures causing atrophy in surrounding areas
what is a common cause of pressure atrophy
decubitus ulcers
what are types of atrophy from inflammatory and immunologic processes
atrophic gastritis, celiac sprue
autoimmune!
what is atrophy senility
senile osteoporosis
aging!
What are the main mechs of atrophy
ubiquitin-proteasome protein breakdown pathway
accelerated proteolysis in catabolic conditions