Cell Injury, Adaption, and Death Flashcards

1
Q

In what ways do cells adapt to chronic stress or insult?

A
hypertrophy
atrophy
hyperplasia
metaplasia
dysplasia
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2
Q

When a myocyte hypertrophies, which components of the cell enlarge?

A

cytoplasm and nucleus

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3
Q

When a bone is in a cast for weeks, in what ways do the cell adapt?

A

disuse atrophy –> decrease in cell size

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4
Q

In Alzheimer’s disease, what kind of atrophy occurs?

What about if there is not enough ACTH produced by adrenal gland?

A

loss of cells
cerebral atrophy
in 80 y/o male, physiological atrophy
adrenal atrophy

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5
Q

T/F: Atrophy can be loss of cells or decrease in cell size.

A

True

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6
Q

What’s hyperplasia? Give an example. What’s the difference between hypertrophy and hyperplasia?

A

The increase in the number of cells - ex: endometrial hyperplasia; hyperplasia is increased number of cells, hypertrophy is enlarged cells

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7
Q

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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8
Q

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

A

psoriasis: epidermal hyperplasia

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9
Q

Increased # of cells from a persistent stress/stimulus

A

hyperplasia

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10
Q

Explain an example of cigarette smoke involving metaplasia?

A

cigarette smoke irritates and causes normal ciliated columnar epithelium to become squamous cells

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11
Q

When one cell type switches to another cell type, usually in response to an injurious process like cigarette smoke or acid reflux into the esophagus.

A

metaplasia

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12
Q

Is metaplasia reversible? If it continues, what could happen?

A

Metaplasia is “usually” reversible if the noxious stressor is removed. If not, then it may go into dysplasia and dysplasia may lead to cancer.

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13
Q

What can reflux from stomach to esophagus cause?

A

glandular metaplasia leading to glandular dysplasia - distal esophagus with squamous epithelium becomes glandular like that of the stomach

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14
Q

How does a normal cell turn into a cancer cell? What is usually the cell stage before cancer?

A

Rarely does a normal cell directly turn into a cancer cell. It will become a hyperplastic or metaplastic cell, a dysplastic cell, and then cancer. The stage before cancer is dysplasia.

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15
Q

If a thrombus causes a vasospasm, what type of necrosis results?

A

ischemic necrosis (coagulative)

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16
Q

An infarct is an area of (blank)

A

necrosis

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17
Q

What’s the difference between necrosis and apoptosis?

A
necrosis = accidental cell death
apoptosis = programmed cell death
18
Q

When there is ischemia, or sudden loss of blood flow, what does this affect on the cellular level? What three things increase inside the cell during cell swelling?

A

halts ATP production
affects ion channels and ion pumps
Na+, Ca+, lactic acid

19
Q

Following an injury, what happens initially? Then, biochemical, ultrastructural, light microscopic changes, and gross morphologic changes occur over time.

A

loss of cell function

20
Q

Necrosis caused by occlusion of vascular supply

A

coagulative necrosis

21
Q

This type of necrosis is seen in the brain and in infections

A

liquefactive necrosis

22
Q

This type of necrosis is seen in tuberculosis - it looks cheesy

A

caseous necrosis

23
Q

This type of necrosis is seen in syphilis

A

gummatous necrosis

24
Q

This type of necrosis is seen in vessel walls in hypertension and vasculitis

A

fibrinoid necrosis

25
What does Ca++ do to mitochondria?
poisons it
26
What is MPT?
mitochondrial permeability transition - it is when pores develop in response to too much Ca++ - causes H+ to flow out and leads to loss of membrane potential and inability to generate ATP
27
What are ROSs? What percentage of molecular oxygen consumed in the mito is converted to ROS?
reactive oxygen species; 5%
28
List some reactive oxygen species generated normally
O2- (superoxide) H2O2 OH-
29
What is oxidative stress?
when reactive oxygen species overwhelms antioxidants
30
What do ROS lead to?
lipid peroxidation ultimately leading to membrane damage
31
Following an infarct, what is the area of savable cells called?
ischemic penumbra
32
When you draw blood, you are looking for enzymes. How are enzymes getting into the blood?
ROS causing lipid peroxidation --> membrane damage --> enzymes leaking into blood
33
What happens to myocardial ischemia with reperfusion (breaking up thrombi)? Does it cause injury? Why is this ok?
allows for smaller final infarct size, but there is still reperfusion injury. This is ok, because it causes more good than harm.
34
What happens when you reoxygenate cells?
reperfusion injury caused by free radicals - mitochondrial perfusion transition
35
What causes reperfusion injury?
oxygen free radicals | Ca++ overload
36
Two forms of apoptosis?
intrinsic | extrinsic
37
During the mitochondrial instrinsic pathway, what happens when you dump cyto C from mito into cell?
start releasing caspases
38
What is the extrinsic (death receptor) pathway?
cytotoxic T cell comes along and binds to TNF receptor and induced cell death
39
What is TNF?
a cytokine
40
Fas binds to FasL and activates the death domain. What pathway is this?
extrinsic pathway
41
With viral hepatitis, what type of cell death occurs? How?
apoptosis - hepatocytes express HLA1. Cytotoxic T cell with FasL recognizes this ligand, causes caspase 8 activation and initiates a caspase cascade
42
What does too much alcohol cause in hepatocytes?
too much fat in hepatocytes -- fatty liver