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
Q

What does Ca++ do to mitochondria?

A

poisons it

26
Q

What is MPT?

A

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
Q

What are ROSs? What percentage of molecular oxygen consumed in the mito is converted to ROS?

A

reactive oxygen species; 5%

28
Q

List some reactive oxygen species generated normally

A

O2- (superoxide)
H2O2
OH-

29
Q

What is oxidative stress?

A

when reactive oxygen species overwhelms antioxidants

30
Q

What do ROS lead to?

A

lipid peroxidation ultimately leading to membrane damage

31
Q

Following an infarct, what is the area of savable cells called?

A

ischemic penumbra

32
Q

When you draw blood, you are looking for enzymes. How are enzymes getting into the blood?

A

ROS causing lipid peroxidation –> membrane damage –> enzymes leaking into blood

33
Q

What happens to myocardial ischemia with reperfusion (breaking up thrombi)? Does it cause injury? Why is this ok?

A

allows for smaller final infarct size, but there is still reperfusion injury. This is ok, because it causes more good than harm.

34
Q

What happens when you reoxygenate cells?

A

reperfusion injury caused by free radicals - mitochondrial perfusion transition

35
Q

What causes reperfusion injury?

A

oxygen free radicals

Ca++ overload

36
Q

Two forms of apoptosis?

A

intrinsic

extrinsic

37
Q

During the mitochondrial instrinsic pathway, what happens when you dump cyto C from mito into cell?

A

start releasing caspases

38
Q

What is the extrinsic (death receptor) pathway?

A

cytotoxic T cell comes along and binds to TNF receptor and induced cell death

39
Q

What is TNF?

A

a cytokine

40
Q

Fas binds to FasL and activates the death domain. What pathway is this?

A

extrinsic pathway

41
Q

With viral hepatitis, what type of cell death occurs? How?

A

apoptosis - hepatocytes express HLA1. Cytotoxic T cell with FasL recognizes this ligand, causes caspase 8 activation and initiates a caspase cascade

42
Q

What does too much alcohol cause in hepatocytes?

A

too much fat in hepatocytes – fatty liver