General Principles of Cell Growth, Injury, & Death Flashcards

1
Q

Generally, pathologic hyperplasia can progress to dysplasia and eventually cancer - what is the major example where this does not apply?

A
  • benign prostatic hyperplasia (BPH); the hyperplasia here is not associated with an increased risk of cancer
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2
Q

How does atrophy occur (3 main mechanisms)?

A
  • apoptosis, autophagy, and degradation of the cytoskeleton (via ubiquitin-proteosomes)
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3
Q

Acid reflux can cause the esophagus’ normal _______ cells to change into ______ cells (which are seen in the stomach); this metaplasia is known as:

A
  • change from squamous cells to columnar cells (columnar cells can better handle the acidic environment)
  • called Barrett’s esophagus
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4
Q

Myosititis Ossificans

A
  • metaplasia in inflamed skeletal muscle

- bony growth is produced in the muscle during healing

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5
Q

Dysplasia

A
  • disorganized cellular growth

- the proliferation of precancerous cells

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6
Q

T or F: Dysplasia, like cancer, is irreversible.

A
  • false!

- dysplasia is reversible, but once it progresses to carcinoma it is irreversible

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7
Q

Slow and constant stress will result in ______; Rapid and strong stress will result in ______.

A
  • slow and constant = atrophy

- rapid and strong = infarction

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8
Q

What is Hypoxia? What are the three main causes?

A
  • hypoxia = low O2 delivery to tissues

- ischemia, hypoxemia, and decreased O2 carrying capacity of the blood are the three main causes

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9
Q

Methemoglobinemia

A
  • when the Fe2+ in Hb becomes Fe3+ (methemoglobin), resulting in the inability of Hb to bind O2
  • gives blood a chocolate-colored tinge
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10
Q

Ischemia can also occur through blockage of the vein, decreasing the flow of fresh blood to the organ. This can occur in the liver in what is known as:

A
  • Bud Kiari Syndrome

- (thrombosis of the hepatic portal vein)

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11
Q

Without O2, what three major events occur in the cell?

A
  • cellular swelling, inappropriate activation of enzymes, and lactic acidosis
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12
Q

Why does cellular swelling occur in hypoxia?

A
  • O2 is needed to form ATP, which is necessary to maintain the Na+-K+-ATPase pump. when this fails, Na+ will accumulate in the cell and will bring in a ton of water with it = swelling
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13
Q

What is the hallmark sign of reversible injury?

A
  • cellular swelling
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14
Q

Why does the inappropriate activation of enzymes occur in hypoxia?

A
  • O2 is needed to form ATP, which is necessary for maintaining low [Ca2+] (a potent enzyme activator) in the cytosol. without ATP, Ca2+ builds up in the cytosol and can freely activate enzymes
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15
Q

What is the hallmark of irreversible injury?

A
  • membrane damage
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16
Q

What is the hallmark of cell death?

A
  • loss of the nucleus
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17
Q

What three events occur in the loss of a nucleus?

A
  • pyknosis –> karyorrhexis –> karyolysis
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18
Q

Pyknosis

A
  • 1st step in loss of nucleus

- the nucleus shrinks

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19
Q

Karyorrhexis

A
  • 2nd step in loss of nucleus

- the nucleus breaks down into large pieces

20
Q

Karyolysis

A
  • 3rd step in loss of nucleus

- the pieces of nucleus are degraded

21
Q

T or F: necrosis is NEVER physiologic, it is ALWAYS pathologic.

A
  • true!
22
Q

6 Sub-types of Necrosis

A
  • coagulative necrosis, liquifactive necrosis, gangrenous necrosis, caseous necrosis, fat necrosis, and fibrinoid necrosis
23
Q

Coagulative Necrosis

A
  • when the necrotic tissue remains firm; the cell shape and organ structure are preserved
24
Q

When is coagulative necrosis seen?

A
  • seen in infarction of all organs EXCEPT the brain
25
Q

What preserves the cellular structure in coagulative necrosis?

A
  • the coagulation of cellular proteins
26
Q

Why doesn’t coagulative necrosis occur in brain infarctions?

A
  • because the brain has mycroglial cells which contain enzymes that break down the cellular components (results in liquifactive necrosis)
27
Q

Liquifactive Necrosis

A
  • when the necrotic tissue becomes liquified

- a result of enzymatic lysis of the cells

28
Q

When is liquifactive necrosis seen?

A
  • seen in brain infarction (due to mycroglial cell enzymes), abscess (due to neutrophil enzymes), and pancreatitis (due to pancreatic enzymes)
29
Q

Gangrenous Necrosis

A
  • coagulative necrosis with mummified (gangrenous) tissue
30
Q

What is “Wet Gangrene”?

A
  • this results when an infection occurs at gangrenous tissue; both liquifactive and gangrenous necrosis will occur
31
Q

When is gangrenous necrosis seen?

A
  • seen in ischemia of the lower limbs
32
Q

Caseous Necrosis

A
  • soft necrotic tissue with a cheese-like appearance

- a combination of coagulative and liquifactive necrosis

33
Q

When is caseous necrosis seen?

A
  • seen in granulomatous inflammation from TB and fungi
34
Q

Fat Necrosis

A
  • when necrosis of adipose tissue occurs

- results in a chalky-white appearance

35
Q

What makes fat necrosis chalky-white?

A
  • the Ca2+ of the dead fat joins with the fatty acids in a process called saponification
36
Q

When is fat necrosis seen?

A
  • seen in trauma to fat (ex: breasts) and in pancreatitis-mediated damage to the peripancreatic fat
37
Q

Fibrinoid Necrosis

A
  • when necrotic damage to the blood vessel wall occurs
38
Q

When is fibrinoid necrosis seen?

A
  • seen in vasculitis and malignant HTN
39
Q

Pre-Eclampsia

A
  • disease of pregnancy (uknown etiology), results in very high HTN and therefore yields fibrinoid necrosis
40
Q

Caspases activate which two enzymes? What does each do?

A
  • proteases: break down the cytoskeleton

- endonucleases: break down the DNA

41
Q

What are the three apoptotic pathways?

A
  • intrinsic mitochondrial pathway, extrinsic receptor-ligand pathway, cytotoxic CD8+ T-cell pathway
42
Q

Intrinsic Mitochondrial Pathway

A
  • a trigger inactivated Bcl2, and the mitochondrial membrane loses its stability, releasing cytochrome c into the cytoplasm and activating caspases
43
Q

Extrinsic Receptor-Ligand Pathway

A
  • Fas-L binds to Fas (CD95) on the target cell, inducing apoptosis
44
Q

Cytotoxic CD8+ T-Cell Pathway

A
  • T-cell binds to target cell and releases perforins (creates a pore) and granzymes to activate caspases
45
Q

What ALWAYS follows necrosis?

A
  • acute inflammation