Parks: Cell Injury, adaption and cell death Flashcards
How should you address a patients inflammation?
What cells are being injured? What is etiology of the injury? Stop the cell/tissue injury Contain the damage Clear/remove the damage cells and tissue Help the tissue repair itself and bring it back to as near normal function as possible
Accidental cell death?
programmed cell death?
necrosis
apoptosis
What are the five different adaptations that can take place after chronic stress or insult?
hypertrophy atrophy hyperplasia metaplasia dysplasia
What hypetrophys in the muscle cell?
the cytoplasm and the nucleus
How should you think about a hypertrophic heart?
think of it as having acute vasoconstriction so not enough blood can get through
What is atrophy?
cells get smaller (can occur with disuse)
What is hypertrophy?
the enlargement of an organ or tissue from the increase in SIZE of its cells.
What is hyperplasia?
increase in number of cells from a persistant stress/stimulus
(blank) is “abnormal” and usually leads to irregular-heavy periods (meno-metrorrhagia) or PMB (post-menopausal uterine bleeding)
endometrial hyperplasia
epidermal hyperplasia is called (blanK)
psoriasis (increased keritanocytes i.e epidermal hyperplasia)
What is this:
Common from anovulatory cycles and unopposed estrogen, the stressor. Persistent uterine bleeding from endometrial breakdown can occur leading to anemia.
endometrial hyperplasia
What is this:
Epidermal hyperplasia from chronic inflammation. Large skin plaques can result.
psoriasis (idiopathic)
What is this an example of:
cigarette smoke in bronchus-> irritates ciliated columnar epithelium -> turn into squamos cells
squamos metaplasia
(blank) is when one cell type switches to another cell type. It’s a cell adaptation.
metaplasia
Is metaplasia reversible?
usually if the noxious stressor is removed, if not then it may go into dysplasia and dysplasia can lead to cancer :(
What does this describe:
gastric reflux turns normal squamos epithelium into glandular epithelium turning into barrett’s esophagus.
metaplasia
What is usually the stage before cancer?
dysplasia
What is this:
the enlargement of an organ or tissue by the proliferation of cells of an ABNORMAL type,
dysplasia
What is the main difference between metaplasia and dysplasia?
dysplasia is irreversible while metaplasia is reversible
What kind of necrosis does ischemia cause?
coagulative (or ischemic) necrosis.
Why is cocaine bad for your blood?
it causes vasospasms and thus obstruction of blood flow which may result in ischemic necrosis or MI via blood clots
What am I talking about:
swelling of ER and mito->breakdown of PM, organelles and nucleus, leakage of contents (i.e. cell explodes due to membrane popping)
necrosis
What am I talking about:
condensation of chromatin
cellular fragmentation
phagocytosis of cell fragments
apoptosis
How come the cell dies without oxygen?
cuz you need it to gain ATP, you get loss of ATP. So anaerobic glycolysis kicks in to compensate and a bunch of hydrogen gets made (lactic acid). So we pump this out of the cell in exchange for sodium. All this sodium inhibits the sodium calcium exchanger so you end up with increased Calcium, sodium. This brings a ton of water into the cell OH NO SWELLING! This increased calcium activates phospholipase which breaks down the membranes. Dead cell
What is super bad about the fact that ischemia causes your cells to take in a lot of sodium, calcium, lactic acid, inorganic phosphate?
it causes water to enter cell and in the brain this is what happen and you stroke out!
What can induce tissue swelling in your liver?
acetaminophen toxicity
When you have an injury, what occurs immediately and what takes time?
pain happens immediately and cell death
biochemical, structural. light microscopic and gross morphological changes take time
How can you get a hemmorhagic infarct?
the blood vessels in the tissue rupture due to lack of oxyen and they will release blood
What is the most common necrosis?
coagulative/ ischemic necrosis (caused by occlusion of vascular supply)
Where do you see liquefactive necrosis?
in the brain and in infections
Where do you see caseous necrosis?
TB
Where do you see gummatous necrosis?
syphilis
Where do you see fibrinoid necrosis?
in vessel walls in hypertensions and vasculitis
An abscess destroys the tissue making a (blank) necrosis.
liquefactive
WHy are infarcts wedge shaped?
because occluded vessel has branches out and these branches are blocked
Why do we hate calcium overload in our cells?
calcium overload results in activation of phospholipase which results in membrane damage and susceptibilty to radicals which destroys the cell
What does MPT stand for?
mitochondrial permeability transition (what happens when you have too much calcium)
will the mito undergo apoptosis or necrosis if it has too much calcium?
either or
It is generally stated that up to (blank) percent of molecular oxygen consumed in the mitochondria is converted to (blank) normally.
5%
ROS
What can ROS’s cause?
lipid peroxidation
How does oxygen become an ROS?
in the electron transport chain, oxygen will steal electron from FMN in complex one and from CoQ in the cytosol-> resulting in superoxide
What does SOD stand for?
What does dismutase mean?
so what does it do?
super oxide dismutase
dismantle
it dismantles superoxide
How do you get free radicals with ischemia?
xanthine oxidase
When someone is ischemic and you reooxygenate them, there are some sucky risks, what are they?
ends up creating more free radicals…. STUPID
What is a good example of an antioxidant system?
glutathionine
What do free radical do?
lipid peroxidation
The area of salvageable or “save able” cells (neurons + glia + blood vessels) is called the ischemic (blank) .
penumbra
What does a cerebral infarct cause?
What dies in a stroke?
stroke
neurons and glia cells
What are reprofusion injuries caused by?
ROS and calcium overload
reperfusion also brings in (blank) and (blank) which contribute to cell injury.
acute inflammatory cells
complements
SO tell me the overall horribleness of ischemia.
get too much Ca which ruins membranes
Reprofuse the area
now you make free radicals which ruins membranes
What happens to the dead or injured cells in a stroke?
some recover w/ reprofusion
BUT many will eventually undergo apoptosis
With (blank) the cell death is orderly and programmed. So the cell contracts and you get little segments of cytoplasm and nucleus and they get phagocytized by surrounding cells or macrophages
apoptosis
Tell me how you undergo intrinisic apoptosis.
DNA damage signals-> sensors-> antagonism of Bcl-2 and activation of Bax, BAK channel-> cytochrom C-> activation of caspases-> cell death
Tell me how you undergo extrinsic apoptosis
TNF or FASL binds with FAS receptor you will activated FADD (Death domain) which will activate caspases and you will get apoptosis
What pathway does viral hepatitis drigger?
apoptosis via FAS ligand and caspases
