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OMK Week 3 > Cell Injury/Death/Adaptation (Cawley) > Flashcards

Cell Injury/Death/Adaptation (Cawley) Flashcards

1
Q

What is Pathology?

A

The study of the structure, function and change in cells and tissues in organs that underlie diseases.

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2
Q

4 steps of the pathological analysis

A
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3
Q

5 ways cells can react to injury?

A
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4
Q

What does persistent stress lead to in a cell?
What are 5 methods of adaptation relief to get the cell back to normal when stressed?
What can reversible cell injury lead to if severe?

A
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5
Q

Describe adaptation response for a myocyte (look at the images too!)
How long does it take a myocyte to undergo necrosis? Causes?

A
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6
Q

Name some etiological agents that can leads to cell injury

A
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7
Q

5 general mechanism of cell injury

A
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8
Q

5 was free radicals can be abnormally unregulated? Three types of activated oxygen

A

O2-, H2O2, -OH

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9
Q

Ionizing radiation can produce a hydroxyl radical through radiolysis. What effect would this have on proliferating cells, and non-proliferating cells?

A
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10
Q

What is the most damaging radical? How could the ferrous iron reaction result in this? What two abnormalities would be needed?

A

Ferrous iron (Fe2+) loses an electron during conversion to the ferric (Fe3+) state.

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11
Q

What are endogenous antioxidants and what are exogenous antioxidants?

A

Antioxidants are compounds that inhibit oxidation

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12
Q

Describe Ca/Mg pump and what happens when disrupted.

A
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13
Q

Describe injurious stimuli effects on membrane damage (3 possible abnormal outcomes) Intracellular Ca and ROS.

A
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14
Q

Worst result in Mitochondrial dysfunction? What is MPT?

A
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15
Q

4 steps (in a way) of acute cellular injury, causing reversible response?

A
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16
Q

ischemia can lead to disruptions in mitochondrial processing, leading to low levels of ATP? What three big responses can happen when ATP levels are low like this during reversible cell injury?

A
17
Q

What makes a cell irreversible injury?

A

PERMANENT Mitochondria damage or cell membrane damage.

18
Q

4 things that could very well mean that irreversible cell injury is happening and not reversible?

A
19
Q

What is the critical factor in cell death?

A

Membrane damage! —-> ATP depletion, Ca+ activation (Proteases phospholipases) and O2 derived free radicals.

20
Q

How long does it take to view a dead cell?

A

it can take hours or even days with even a microscope. The enzymes take time to break down and burn things! But it is already way past committed so they is no stopping it! Even with terrible infarction in the heart, if a patient were to die and you immediately checked his heart there would be no notable changes, until hours, maybe days.

21
Q

Summary, just peep it! :)

A
22
Q

Necrosis vs Apoptosis?

A
23
Q

Just for an idea (I do not think this is stressed) describe necroptosis and Pyroptosis?

A
24
Q

Two major types of necrosis, other common types? (5) total

A
25
Q

White tissue in the heart?

A

Scar tissue

25
Q

White tissue in the heart?

A

Scar tissue

26
Q

What should you think with Caseous Necrosis?

A

TB, until proven otherwise, needing micro bacterium and fungal. Invaders are usually these two things in nature.

27
Q

Apoptosis? Physiological or pathological? Gene regulation? Inflammation? Morphology?

A
28
Q

Apoptosis Pathology examples? (5)

A

DNA damage, Accumulation of misfiled proteins, Cytotoxic T cells in transplants, Viral hepatitis, and atrophy in gland with blocked duck.

29
Q

Necrosis vs Apoptosis: Cells, mechanisms, inflammation, DAMPs/PAMPs

A
30
Q

Chronic cell injury; explain lysosomal auto-Nagy

A
31
Q

What is Steatosis? Where is it most common? Most common cause?

A

Steatosis is fatty change, most commonly in the liver. Alcohol is the most common cause, decreased fatty acid oxidation.

32
Q

How do you go from alcohol to cirrhosis?

A
33
Q

What are Hyperplasia, Hypertrophy, Atrophy and Metaplasia

A

Hyperplasia - increase in number of cells
Hypertrophy - increase in size of cells
Atrophy - Cell size decreases
Metaplasia - One benign cell type to another benign cell type

34
Q

Where wound you find liquefactive necrosis?

A

Abscesses, also only type of necrosis seen in the brain.

35
Q

Hypertrophy Physiological and Pathological changes?

A
36
Q

Atrophy Physiological and Pathological

A
37
Q

Describe metaplasia

A

OMK Week 3 (3 decks)

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