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Flashcards in Cell Injury and Death Deck (53):
1

Homeostasis of Cells

Steady State
Cells - Maintaining a stable internal environment
Cells adjust and try to maintain
Some adjustments are normal and others are pathological

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Cellular Aging

Loos of ability of a cell to divide

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Reasons for Cellular Aging

Genetics - predetermines aging of your cells
Free Radical Theory - can lead to pathology
Telomere Clock Theory - lose telomeres as we age and we only have a certain number of them

4

Stressors - Normal

We have normal responses to stressors
Cold - shiver - move blood around so small level of ischemia in some muscles - short term adjustment of our cells - just an adaptation, not damage

5

Stressor - Hypoxia

Reduced O2 delivery to tissue
Ischemia, Loss of arterial blood flow to reach target
Can lead to occlusion of arterial circulation
Shunting
Failure of heart to pump - too large
Occlusion of veins
O2 can't diffuse into tissue and CO can't diffuse away

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Stressor - Hypoxemia

Decrease of deficient O2 in blood
- Too little O2 in atmosphere
- Failure to ventilate
- Failure to oxygenate
- Failure to carry O2
- Anemia, Carbon Monoxide poisoning

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Initial Indication that cell is injured

Cellular Swelling
Can be caused by Hypoxia - decrease in mitochondrial phosphorylation (absent or decline in ATP production)
Results in failure of NA/K pump

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Stressor - Chemical

Drugs, heavy metals, cleaning solutions, dyes
Interaction damages the plasma and ER membrane
Leads to lipid accumulation within cell and cellular swelling (allows large molecules to move into the cell)

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Stressor - Physical

Trauma
Temp extremes
Ionizing (chemo) radiation
Pressure (aquatic therapy)
Electrical energy
Mechanical energy (prolonged loud noises damage ear)

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Stressor - Microorganisms

Bacteria
Viruses
Fungi
Parasites
They all have different role and produce different things

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Stressor - Immunologic Reactions

How vigorous inflammatory response will be, depends on how in tune immune system is
- Mediators of inflammation
- Auto-immune reactions

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Stressor - Genetic Defects not allowing cells to adapt

- Alternation in chromosome structure
- Single gene mutations resulting in protein abnormalities
- Multi gene mutations

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Stressor - Nutritional/Metabolic Imbalances

- Leads to dec. or impaired cellular function

14

Stressor - Free Radicals

- Molecules generated in a variety of circumstances (cant stop generation of free radicals)
- Single unpaired electron that can bond with other molecules and produce detrimental effects on cells
- Oxidative stress or reactive oxygen species - the more free radicals - the more oxidative stress - inflammation produces a lot

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Adaption - cells reaction to stressor

How we adapt depends on duration, manner in which it came about, and severity of stressor, type of cell that has been injured and state that it was in at time of injury
Cells that produce quickly tend to adapt faster

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Adaptation - Atrophy

Decrease or shrinkage in size of the cell
Loss of cell substances, including mito, myofilament, and ER

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Adaptation - Common Causes of Atrophy

1. Decreased workload
2. Loss of innervation
3. Decrease blood supply
4. Loss of endocrine stimulation
5. Aging

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Hypertrophy

- Increase in the size of the cell
- Increase in protein synthesis with accumulation of proteins
- Increase # and size of intracellular organelles
- Generally implies an increase in cellular metabolic activity

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Hyperplasia

- Increase in the number of cells
- Can be pathological too
- Divided into two types
1. Physiological = breast enlargement secondary to puberty or pregnancy
2. Compensatory = liver regeneration

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Metaplasia

- One adult cell type is replaced with another adult cell type

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Most Common Metaplasia

Epithelial cells being replaced by mesenchymal cells

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Metaplasia Examples

Respiratory Tract - smokers - columnar to epithelial
Muscle - muscle fibers ossify - abnormal

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Dysplasia

- Derranged development
- Loss of normal orientation of one cell to another
- Alterations in size/shape of cell, nuclear size/shape, and staining characteristics
- Often genetic component - PRE CANCEROUS
- NOT considered an adaptive change but might be reversible with therapy

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Apoptosis

Normal programmed cell death (house cleaning)
Cells shrink and the nuclei condenses
DNA breaks down into fragments
Not injurious to tissue and will not produce inflammation

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Cell Necrosis

Cell Death
Injurious to tissue
Always pathological
Will produce inflammation

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Apoptosis and Blebs

Outpouching of structure filled with blood or air
Can get bigger and explode - spontaneous pneumothorax
- Taken care of normally with phagocytosis

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Necrosis and Blebs

Gets bigger and bigger and ruptures the cell
Some lytic agents might be released and then lead to inflammatory response

28

Cellular Swelling

- Indicator of cell injury
- Remain within the range of homeostasis
- Still reversible at this stage
- Na/K pump is opening and allowing influx of water - this results in structure (mitochondria) to lose ability to create energy - accumulation of waste products can lead to irreversible injury

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Fatty Changes

- Within range of cell homeostasis and reversible to a degree
- Different lipids within cytoplasm
- Results from an imbalance btw uptake, utilization, and secretion of fat
- Cell can't synthesize lipids and keeps accumulating them until point point of no return

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Irreversible Cell Injury

- Lysosomes - lytic enzymes kill the cell from within
Cytoskeleton starts to thicken and become sclerotic (hard)

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Hallmark for irreversible cell damage / cell death

A lot of Ca going into the cell

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Irreversible Cell Changes

- Progressive degenerative changes occur within the cell
- The nucleus degenerates and dissolves
- Mitochondria cease function
- Massive influx of Ca ions
- Not as adaptable to change in shape

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Cell Death

- Cells are fragmented and are removed
- Sometimes that cytoplasm coagulates and the outer shell takes on Ca deposits - the cell membrane that hardened will line itself with Ca and will develop a shell of Ca (Ca deposit)

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Accumulation Patterns of Cell Injury

- Under certain conditions the cell will accumulate substances within the cytoplasm
- These might be short or long term (more permanent)
- Lipids, glycogen...

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Patterns of Accumulation

Normal but excessive
Abnormal - something that shouldn't be in the cells
Pigments - melanin - sunburns, suntan, freckles...injurious to skin

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Pigments

Communicate injury to the cell
Melanin = thick suntan
Hemosiderin = bruises
Lipofuscin = Liver spots
Bilirubin = jaundice

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Stages of a bruise

1. Red/Blue - hemoglobin (immediate to 2 days)
2. Green/Blue - bilirubin and biliverdin (2-4 days)
3. Yellow/Brown - hemosiderin (3-4 days)

38

Caveat to stages of bruise

research says that visual estimation is accurate only 50% of the time
Secondary to where bruise is located and how deep the injury is

39

PT and bruising

Need to be aware of where they are in the healing process
Whether there is still active bleeding in the tissue you are seeing

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Calcium

- Occurs with Ca influx into dead or dying cells
- Seen most often in cardiovascular and skeletal system
- Mitochondria and ER released their stored Ca which is emptied into extracellular environment

41

Tissue Necrosis

- Refers to outcome of cell death
- Only in living (dead = decay)
- Autolysis action (requires autolytic activity within you)

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Tissue Necrosis Includes

1. Nuuclear changes and fragmentation
2. Membrane rupture
3. Cessation of cell function

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-lysis

Dissolution or decomposition
Autolysis (used in some treatments for wondcare), self digestion of tissue

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Coagulative Necrosis

Most common type of necrosis
Structure is maintained so you can tell what you are looking at
Denaturation of proteins
Associated with ischemia (most common)
AKA ischemic necrosis
Surrounding tissue undergoes inflammation

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Liquefactive

- Dissolution of tissues as a result of hydrolysis
- Softening and liquefaction of tissues
- Common cause is inflammatory reaction
- Cellular digestion by hydrolytic enzyme (dead cells, inflammatory cells, pathogens)

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Liquefactive is most common in

Nervous tissue

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Caseous

Both coagulative and liquefactive necrosis
TB is example
Also seen in fungal infections
Starts to look like cheese in structures with spots

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Fat Necrosis

- Form of liquefactive necrosis that occurs in adipose tissue (breast and pancreas)
- Commonly due to release of lytic enzymes
- May appear chalky white or soap like, feels slimy but is solid

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Gangrene

Visible Necrosis

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Dry Gangrene

Ischemic or Coagulative

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Wet Gangrene

Liquefactive

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Gas Gangrene

Caused by clostridia bacteria
- huge production of gas

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PT Gangrene

How much visible tissue is under/near it?
- Need to get rid of it
- Big toe inflamed - inflammatory response is occurring in the tissue that hasn't necrosed yet so need to get rid of necrosed tissue to prevent further damage to the surrounding tissue