Cellular Adaptation, Injury, and Death Flashcards

1
Q

An adults body contains —– water, as compared to a child with —— water

A

50-65%, 75%

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2
Q

All forms of disease begin with?

A

Alteration in the cells

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3
Q

Atrophy

A

A decrease or shrinkage in cellular size.
Can affect any organ.

Caused by decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation.
Ex. The brain decreasing in size from the aging process.

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4
Q

Hypertrophy

A

An increase in the size of the cell and even in the organ itself.
The heart and kidneys are especially prone to enlargement.
Cellular fluid is not increased, but rather the cellular components.
Caused by hormonal stimulation and increased functional demand.
Ex. the muscles increasing in size from heavy work.
Ex. a kidney is removed and the remaining kidney increases in size to accommodate for the increased demand.
Ex. the uterus and mammary glands increase in size from hormonal stimulation of pregnancy.
Ex. hypertrophy in the heart secondary to hypertension or diseased heartvalves

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5
Q

Hyperplasia

A

An increase in the number of cells as a result of increased cellular division.
Usually a regenerative process. Cannot occur in nondividing cells.
Compensatory hyperplasia enables certain organs, like the liver, to regenerate lost tissue.
Nerve, skeletal muscle, and myocardial cells cannot regenerate.
Hormonal hyperplasia occurs only in estrogen-dependent organs like the uterus and breast.
Pathologic hyperplasia is usually in repsonse to excessive hormonal stimulation or growth factors on target cells.

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6
Q

Dysplasia: Not a True Adaptive Change

A

Abnormal change in size, shape, and organization of mature cells.
Related to hyperplasia and is also known as atypical hyperplasia.
Often encountered in epithelial tissue of the cervix and respiratory tract.
Although strongly associated with the presence of cancerous cells, dysplasia does not indicate cancer and may not progress to cancer.
If the cause is removed dysplastic changes are often reversible.

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7
Q

Metaplasia

A

the reversible replacement of one mature cell type by another, sometimes less differentiated, cell type.
Ex. the replacement of ciliated comlumnar epithelial cells of the respiratory tract with stratified squamous epithelial cells.
These new cells no longer have the mechanical functionality that the old cells did, and cannot sweep debris and mucous out of the bronchial airway.

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8
Q

When does cellular injury occur?

A

When the cell is no longer able to maintain homeostasis.

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9
Q

The single most common form of cellular injury.

A

Hypoxia, a lack of sufficient oxygen.

The most common cause of hypoxia is ischemia.

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10
Q

The form of injury caused by free radicals, specifically known as reactive oxygen species.

A

Oxidative stress.

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11
Q

Free radicals (ROS) are capable of injuring……

A

the chemical bonds formed in proteins, lipids, and carbohydrates.
All of these are key molecules in the cell membranes and nucleic acids.
They are highly reactive, and capable of reacting with most molecules around them.

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12
Q

How are free radicals initiated?

A

Extreme sources of energy, like UV light or radiation.
Activation of endogenous reactions by systems involved in electron transport, like reduction of oxygen to water, redox
Enzymatic metabolism of exogenous chemicals or drugs, cigarette smoke, and other pollutants or drugs.

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13
Q

How can free radicals cause damage?

A

Lipid peroxidation: the same process that turns fat rancid. Causing damage to the membrane and making it more permeable.
Protein alterations. causing fragmentation of polypeptide chains.
DNA fragmentation, causing decreased protein synthesis.
MItochondrial damage, causing the liberation of calcium into the cytosol.

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14
Q

How can free radicals be terminated?

A

Antioxidant Enzymes: these block, inactivate, convert and decompress free radicals.
Endogenous: Superoxide dismultase, Glutathione, and Catalase.
Exogenous: Vitamins C, E, A <==== Very easy to use

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15
Q

Necrosis

A

Is the sum of cellular changes after local cell death and the process of cellular self digestion, known as autolysis or autodigestion.
Cells die long before any necrotic changes are noted under light microscope.
Notable changes in the cell: Swelling of the organelles and clumping of chromatin. The cell membrane disintegrates and the contents of the cell are released.
Cell death is disorganized and messy.

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16
Q

What are the four main types of necrosis?

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis

There is also Gangrenous necrosis, which includes gas gangrene

17
Q

Coagulative Necrosis

A

Occurs primarily in the kidneys, heart and adrenal glands.
Commonly caused by hypoxia as a result of severe ischemia. Coagulation is caused by protein denaturation, which causes the protein albumin to change from a gelatinous, transparent state to a firm, opaque state.

18
Q

Liquefactive Necrosis

A

Results from ischemic injury to neurons and glial cells in the brain.
Hydrolytic enzymes within the cells of the brain are released and being digesting themselves. This turns the tissue to a soft, liquid state, which then segregates from healthy tissues forming cysts.

Can also be caused by bacteria: Especially Streptococci, Staphylococci, and Esherichia coli.

19
Q

Caseous Necrosis

A

Usually results from tuberculous pulmonary infection, epsecially Mycobacterium tuberculosis.
This necrosis is a combination of coagulative and liquefactive necroses.
The cells disintegrate, but the debris is not completely digested by the hydrolases.
Tissues resemble clumped cheese, soft and grandular.
A granulomatous inflammatory wall encloses areas of caseous necrosis.

20
Q

Fatty Necrosis

A

Involves the cellular dissolution caused by powerful enzymes called lipases.
These can occur in the beasts, pancreas, and other abdominal structures.
Fatty acids are released by the lipases, and combine with calcium, magnesium, and sodium ions, creating soaps.
Necrotic tissue appears opaque and chalk white.

21
Q

Gangrenous Necrosis

A

Results from severe hypoxic injury.
Commonly caused by arteriosclerosis, or blockage, of major arteries, particularly those of the lower legs.
With a combination of hypoxia and subsequent bacterial invasion, the tissues can undergo necrosis.
Dry gangrene usually involves coagulative necrosis.
The skin becomes very dry and shrinks, resulting in wrinkles, and its color changes to dark brown or black.
Wet gangrene develops when neutrophils invade the site, causing liquefactive necrosis. Usually occurring in internal organs, causing the site to become cold, swollen, and black. A foul odor is present, and it becomes sytemic death can follow.

22
Q

Gas Gangrene

A

Caused by tissue infection of one of many types of Clostridium. These anaerobic bacteria produce hydrolytic enzymes and toxins that destroy connective tissue and cellular membranes and cause bubbles of gas to form in muscle cells.
If RBC become lysed in this process then death is a possible result.

23
Q

Apoptosis

A

Programmed cell death.
Very organized.
Cells need to die, otherwise, endless proliferation would lead to gigantic bodies.
10 billion new cells a day, and then destroy the same number
When cell injury exceeds repair mechanisms, the cell triggers apoptosis.
Cell death occurs cleanly and neatly.

24
Q

Autophagy

A

Eating of self. This process is carried out in cell that are being starved of appropriate nutrients. This process allows the cell to reuse digested material.
Autophagy can maintain cellular metabolism under starvation conditions and remove damaged organelles under stress conditions, improving the survival of cells.
Forms a double membrane autophagosome around organelle to be digested. Which then fuses with a lysosome.
The process is the “garbage” collecting system of the cell.