Cell Responses to Injury Flashcards

1
Q

Reversible; cell gets bigger (no new cells!)

A

hypertrophy

ex/ uterus during pregnancy!

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2
Q

Reversible; increase in number of cells

A

hyperplasia

may be precancerous, or may be normal - like during period

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3
Q

Two basic ways to get hyperplasia:

A

1) growth factor

2) stem cells

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4
Q

Cyclosporin is a medication that can cause:

A

hyperplasia

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5
Q

Occurs in tissues that are incapable of cell division

A

hypertrophy

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6
Q

Reversible; changes in ion concentration & water influx

A

hydropic swelling

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7
Q

When nuclear membrane starts to break down:

A

karyorrhexis

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8
Q

When there is continuous injury, the nucleus becomes dark purple and looks like shriveled raisin. This is called:

A

pyknosis

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9
Q

When the nucleus totally breaks up:

A

karyolysis

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10
Q

Increase in cell volume characterized by pale cytoplasm and normal nucleus

A

hydropic swelling

reflection of acute, reversible injury

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11
Q

When cells aren’t able to maintain membrane and the contents leak out:

A

necrosis

elicits an inflammatory response

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12
Q

What are the six types of necrosis? (CCFFGL)

A
  • Coagulative
  • Caseous
  • Fat
  • Fibrinoid
  • Gangrenous
  • Liquefactive
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13
Q

Type of necrosis that preserves the architecture of the tissue

A

Coagulative

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14
Q

Type of necrosis associated with TB

A

Caseous

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15
Q

Type of necrosis where there is leakage of enzymes into abdomen

A

Fat

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16
Q

Type of necrosis that can be seen in oral cavity, and it is immunologically mediated vasculitis in blood vv walls

A

Fibrinoid

17
Q

Type of necrosis that involves both coagulation and liquefaction

A

Gangrenous

18
Q

Type of necrosis that occurs with cerebral infarction and bacterial infections

A

Liquefactive

19
Q

What is the type of necrosis that occurs in heart attacks?

A

Coagulative necrosis

20
Q

Type of necrosis where pus is seen

A

Liquefactive

21
Q

When mitochondria doesn’t get enough oxygen, what happens to ATP levels?

A

Decrease

low oxidative phosphorylation = low ATP

22
Q

Ischemia changes are reversible or irreversible?

A

Reversible! But must be taken care of quickly

23
Q

Why is apoptosis preferred and not necrosis?

A

Necrosis -> releases cell contents; INFLAMMATION

Apoptosis -> cells break down in packets so contents stay contained; NO inflammation

24
Q

Too much calcium in the cell disrupts:

A

ATP generation, so apoptosis is induced because damaging enzymes are activated

25
Q

What ROS can cause pathologic effects, like membrane damage or mutations?

A

OH (hydroxyl radical)

26
Q

Hypoxia vs. Ischemia?

A
Hypoxia = deficiency of oxygen
Ischemia = loss of blood supply, which causes lack of oxygen (more severe than hypoxia)
27
Q

What enzymes are activated in apoptosis?

A

caspases

28
Q

Mitochondrial intrinsic pathway for apoptosis is more common. It is run by a group of effectors called:

A

BCL-2

29
Q

TNF receptor + Fas =

A

Apoptosis

they’re in extrinsic pathway

30
Q

Between necrosis and apoptosis, what is the main difference in regards to loss of plasma membrane?

A

Loss of plasma membrane occurs first in necrosis & last in apoptosis

31
Q

Killer lymphocytes inject ____ through perforin

A

granzyme

32
Q

What is the cell death rheostat?

A

BCL-2