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Block 4 week 2 Dani > Parks: Cell Injury, adaption and cell death > Flashcards

Parks: Cell Injury, adaption and cell death Flashcards

1
Q

How should you address a patients inflammation?

A 
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
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2
Q

Accidental cell death?

programmed cell death?

A

necrosis

apoptosis

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3
Q

What are the five different adaptations that can take place after chronic stress or insult?

A 
hypertrophy
atrophy
hyperplasia
metaplasia
dysplasia
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4
Q

What hypetrophys in the muscle cell?

A

the cytoplasm and the nucleus

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5
Q

How should you think about a hypertrophic heart?

A

think of it as having acute vasoconstriction so not enough blood can get through

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6
Q

What is atrophy?

A

cells get smaller (can occur with disuse)

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7
Q

What is hypertrophy?

A

the enlargement of an organ or tissue from the increase in SIZE of its cells.

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8
Q

What is hyperplasia?

A

increase in number of cells from a persistant stress/stimulus

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9
Q

(blank) is “abnormal” and usually leads to irregular-heavy periods (meno-metrorrhagia) or PMB (post-menopausal uterine bleeding)

A

endometrial hyperplasia

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10
Q

epidermal hyperplasia is called (blanK)

A

psoriasis (increased keritanocytes i.e epidermal hyperplasia)

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11
Q

What is this:
Common from anovulatory cycles and unopposed estrogen, the stressor. Persistent uterine bleeding from endometrial breakdown can occur leading to anemia.

A

endometrial hyperplasia

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12
Q

What is this:

Epidermal hyperplasia from chronic inflammation. Large skin plaques can result.

A

psoriasis (idiopathic)

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13
Q

What is this an example of:

cigarette smoke in bronchus-> irritates ciliated columnar epithelium -> turn into squamos cells

A

squamos metaplasia

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14
Q

(blank) is when one cell type switches to another cell type. It’s a cell adaptation.

A

metaplasia

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15
Q

Is metaplasia reversible?

A

usually if the noxious stressor is removed, if not then it may go into dysplasia and dysplasia can lead to cancer :(

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16
Q

What does this describe:

gastric reflux turns normal squamos epithelium into glandular epithelium turning into barrett’s esophagus.

A

metaplasia

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17
Q

What is usually the stage before cancer?

A

dysplasia

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18
Q

What is this:

the enlargement of an organ or tissue by the proliferation of cells of an ABNORMAL type,

A

dysplasia

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19
Q

What is the main difference between metaplasia and dysplasia?

A

dysplasia is irreversible while metaplasia is reversible

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20
Q

What kind of necrosis does ischemia cause?

A

coagulative (or ischemic) necrosis.

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21
Q

Why is cocaine bad for your blood?

A

it causes vasospasms and thus obstruction of blood flow which may result in ischemic necrosis or MI via blood clots

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22
Q

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)

A

necrosis

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23
Q

What am I talking about:
condensation of chromatin
cellular fragmentation
phagocytosis of cell fragments

A

apoptosis

24
Q

How come the cell dies without oxygen?

A

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

25
Q

What is super bad about the fact that ischemia causes your cells to take in a lot of sodium, calcium, lactic acid, inorganic phosphate?

A

it causes water to enter cell and in the brain this is what happen and you stroke out!

26
Q

What can induce tissue swelling in your liver?

A

acetaminophen toxicity

27
Q

When you have an injury, what occurs immediately and what takes time?

A

pain happens immediately and cell death

biochemical, structural. light microscopic and gross morphological changes take time

28
Q

How can you get a hemmorhagic infarct?

A

the blood vessels in the tissue rupture due to lack of oxyen and they will release blood

29
Q

What is the most common necrosis?

A

coagulative/ ischemic necrosis (caused by occlusion of vascular supply)

30
Q

Where do you see liquefactive necrosis?

A

in the brain and in infections

31
Q

Where do you see caseous necrosis?

A

TB

32
Q

Where do you see gummatous necrosis?

A

syphilis

33
Q

Where do you see fibrinoid necrosis?

A

in vessel walls in hypertensions and vasculitis

34
Q

An abscess destroys the tissue making a (blank) necrosis.

A

liquefactive

35
Q

WHy are infarcts wedge shaped?

A

because occluded vessel has branches out and these branches are blocked

36
Q

Why do we hate calcium overload in our cells?

A

calcium overload results in activation of phospholipase which results in membrane damage and susceptibilty to radicals which destroys the cell

37
Q

What does MPT stand for?

A

mitochondrial permeability transition (what happens when you have too much calcium)

38
Q

will the mito undergo apoptosis or necrosis if it has too much calcium?

A

either or

39
Q

It is generally stated that up to (blank) percent of molecular oxygen consumed in the mitochondria is converted to (blank) normally.

A

5%

ROS

40
Q

What can ROS’s cause?

A

lipid peroxidation

41
Q

How does oxygen become an ROS?

A

in the electron transport chain, oxygen will steal electron from FMN in complex one and from CoQ in the cytosol-> resulting in superoxide

42
Q

What does SOD stand for?
What does dismutase mean?
so what does it do?

A

super oxide dismutase
dismantle
it dismantles superoxide

43
Q

How do you get free radicals with ischemia?

A

xanthine oxidase

44
Q

When someone is ischemic and you reooxygenate them, there are some sucky risks, what are they?

A

ends up creating more free radicals…. STUPID

45
Q

What is a good example of an antioxidant system?

A

glutathionine

46
Q

What do free radical do?

A

lipid peroxidation

47
Q

The area of salvageable or “save able” cells (neurons + glia + blood vessels) is called the ischemic (blank) .

A

penumbra

48
Q

What does a cerebral infarct cause?

What dies in a stroke?

A

stroke

neurons and glia cells

49
Q

What are reprofusion injuries caused by?

A

ROS and calcium overload

50
Q

reperfusion also brings in (blank) and (blank) which contribute to cell injury.

A

acute inflammatory cells

complements

51
Q

SO tell me the overall horribleness of ischemia.

A

get too much Ca which ruins membranes
Reprofuse the area
now you make free radicals which ruins membranes

52
Q

What happens to the dead or injured cells in a stroke?

A

some recover w/ reprofusion

BUT many will eventually undergo apoptosis

53
Q

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

A

apoptosis

54
Q

Tell me how you undergo intrinisic apoptosis.

A

DNA damage signals-> sensors-> antagonism of Bcl-2 and activation of Bax, BAK channel-> cytochrom C-> activation of caspases-> cell death

55
Q

Tell me how you undergo extrinsic apoptosis

A

TNF or FASL binds with FAS receptor you will activated FADD (Death domain) which will activate caspases and you will get apoptosis

56
Q

What pathway does viral hepatitis drigger?

A

apoptosis via FAS ligand and caspases

Block 4 week 2 Dani (8 decks)

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