Ch. 2 Stress, Injury, and Aging Flashcards

1
Q

Atrophy

A

Decrease in cell size and oxygen consumption in adverse conditions (or decreased demands)

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2
Q

How is atrophy related to insulin/insulin-like growth factor-1?

A

Muscles are maintained by insulin/IGF-1, so if levels are low then muscle atrophy will occur by the ubiquitin-protease system or apoptosis

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3
Q

5 Causes of atrophy

A
  1. Disuse
  2. Denervation (paralysis)
  3. Loss of endocrine stimulation (menopause)
  4. Inadequate nutrition
  5. Ischemia
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4
Q

Hypertrophy

A

Increase in cell size and tissue mass from increased workload

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5
Q

When does hypertrophy occur?

A

Normal (exercise) or pathologic

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6
Q

What is an example of adaptive hypertrophy?

A

urinary bladder thickens when urinary outflow is obstructed
Myocardial hypertrophy from valvular heart disease or HTN

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7
Q

What is an example of compensatory hypertrophy?

A

When a remaining organ/tissue becomes larger after part of it is removed or becomes inactive
After a kidney removal, the remaining becomes larger to compensate.

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8
Q

How is hypertrophy initiated?

A

ATP depletion, stretching of muscle fibers, activation of cell degradation products, and hormones.

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9
Q

Hyperplasia

A

Increase in number of cells in an organ or tissue capable of mitotic division like the epidermis, intestinal epithelium, and glands

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10
Q

How is hyperplasia initiated?

A

Genes that control cell proliferation are activated
Intracellular messengers that control cell replication are present

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11
Q

What are the two types of physiologic hyperplasia?

A
  1. Hormonal (breast and uterine enlargement during pregnancy from estrogen stimulation)

2.Compensatory (regeneration of liver after partial hepatectomy)

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12
Q

What causes nonphysiologic hyperplasia?

A

Excess hormone stimulation or growth factors
Example: excessive estrogen production causes endometrial hyperplasia
Benign prostatic hyperplasia may be related to androgens
Skin warts caused by growth factors produced by papillomaviruses

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13
Q

Metaplasia

A

When an adult cell type is replaced by another cell type

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14
Q

What causes metaplasia?

A

Response (undifferentiated stem cell reprogramming) to chronic inflammation and is an adaptation for tissue to survive a harsh environment

example: columnar ciliated epi cells are replaced by stratified squamous epi cells in the trachea and bronchi of smokers which can better survive smoke but the protective function of cilia is lost

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15
Q

Dysplasia

A

Deranged cell growth of a specific tissue resulting in cells of varying size, shape, and organization

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16
Q

What causes dysplasia?

A

Chronic irritation and inflammation

17
Q

What are the most common examples of dysplasia?

A

-metaplastic squamous epithelium of respiratory tract and cervix

18
Q

How does dysplasia relate to cancer?

A

It may be a precursor for cancer with incremental cellular changes
BUT it is adaptive and can revert!

(this is what an abnormal pap test detects)

19
Q

What is fatty liver disease?

A

Intracellular accumulation of triglycerides (liver cells usually have some fat that is oxidized for energy use or stored as triglycerides. Fat is released from adipose tissue. Delivery of free fatty acids to the liver is increased in diabetes mellitus (enzyme hormone sensitive lipase is usually inactivated with binding of insulin) and starvation, and in alcoholism lipid metabolism is disturbed.

20
Q

What is jaundice an example of?

A

Endogenous bile pigment accumulation (bilirubin)

21
Q

Dystrophic calcification

A

Calcium salt deposits in injured tissue (heart valve calcifications and advanced atherosclerosis)

22
Q

Metastatic calcifiation

A

Calcium salt deposits in normal tissue due to hypercalcemia

23
Q

What are causes of cell injury?

A

Physical, radiation, chemical. biologic agents, and nutritional imbalances

24
Q

How does hypoxia lead to cell injury?

A

It causes ATP depletion due to lowered ECT activity

25
Q

How does calcium influx cause cell damage?

A

Calcium leaks out of smooth ER and enters the mitochondria and nucleus, causing DNA damage and mitochondrial permeability in transition pores. This allows cytochrome c to enter the cytosol, which has a role in apoptosis. Also activates enzymes such as proteases.

26
Q

How do free radicals lead to cell injury?

A

Free radicals have an unpaired electron and are highly unstable. They set off chain reactions resulting in more free radicals. Damages cell membranes, inactivates enzymes and damages nucleic acids.

27
Q

What are 2 patterns of reversible cell injury?

A

Cell swelling and fatty change

28
Q

What is necrosis?

A

cell death in an organ or tissue in a living person

29
Q

Liquefaction necrosis

A

Some cells die but their catalytic enzymes are not destroyed (softening of center of abscess with discharge of its contents)

30
Q

Coagulation necrosis

A

Acidosis denatures enzymes and structural proteins (hypoxia and infarction - lactic acid!)

31
Q

Infarction

A

Artery becomes occluded and no other source of blood exists for an organ or tissue

32
Q

Caseous necrosis

A

a form of coagulation necrosis where dead cells persist and form a debris (TB granulomas)

33
Q

Gangrene

A

A considerable mass of tissue becomes necrotic

34
Q

What is dry gangrene?

A

Tissue becomes dry, wrinkled, and black. results from interference with arterial blood supply to a part of body with venous return (arteriosclerosis, diabetes)

-line of demarcation
-black in color due to hemoglobin release from lysed RBCs, which turns into iron sulfide when it interacts with hydrogen disulfide made by bacteria
-type of coagulation necrosis

35
Q

What is wet gangrene?

A

Area is cold, swollen, and pulseless. Skin is moist, black, and under tension. Liquefaction and foul odor. Caused by interference with venous return from the affected part and bacterial invasion.

36
Q

What is the programmed aging theory?

A

Changes that occur with aging are genetically programmed.

37
Q

What is the damage or errors aging theory?

A

Changes happen because random events and enviro agents cause DNA damage.