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FS Exam 3 > Cell Injury and Death > Flashcards

Cell Injury and Death Flashcards

(53 cards)

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1
Q

Homeostasis of Cells

A

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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2
Q

Cellular Aging

A

Loos of ability of a cell to divide

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3
Q

Reasons for Cellular Aging

A

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

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4
Q

Stressors - Normal

A

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

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5
Q

Stressor - Hypoxia

A

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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6
Q

Stressor - Hypoxemia

A

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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7
Q

Initial Indication that cell is injured

A

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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8
Q

Stressor - Chemical

A

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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9
Q

Stressor - Physical

A 
Trauma
Temp extremes
Ionizing (chemo) radiation
Pressure (aquatic therapy)
Electrical energy
Mechanical energy (prolonged loud noises damage ear)
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10
Q

Stressor - Microorganisms

A 
Bacteria
Viruses
Fungi
Parasites
They all have different role and produce different things
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11
Q

Stressor - Immunologic Reactions

A

How vigorous inflammatory response will be, depends on how in tune immune system is

  • Mediators of inflammation
  • Auto-immune reactions
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12
Q

Stressor - Genetic Defects not allowing cells to adapt

A
  • Alternation in chromosome structure
  • Single gene mutations resulting in protein abnormalities
  • Multi gene mutations
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13
Q

Stressor - Nutritional/Metabolic Imbalances

A
  • Leads to dec. or impaired cellular function
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14
Q

Stressor - Free Radicals

A
  • 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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15
Q

Adaption - cells reaction to stressor

A

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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16
Q

Adaptation - Atrophy

A

Decrease or shrinkage in size of the cell

Loss of cell substances, including mito, myofilament, and ER

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17
Q

Adaptation - Common Causes of Atrophy

A
  1. Decreased workload
  2. Loss of innervation
  3. Decrease blood supply
  4. Loss of endocrine stimulation
  5. Aging
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18
Q

Hypertrophy

A
  • 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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19
Q

Hyperplasia

A
  • 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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20
Q

Metaplasia

A
  • One adult cell type is replaced with another adult cell type
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21
Q

Most Common Metaplasia

A

Epithelial cells being replaced by mesenchymal cells

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22
Q

Metaplasia Examples

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A

Respiratory Tract - smokers - columnar to epithelial

Muscle - muscle fibers ossify - abnormal

23
Q

Dysplasia

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A
  • 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
24
Q

Apoptosis

Study These Flashcards
A

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

25
Cell Necrosis
Cell Death Injurious to tissue Always pathological Will produce inflammation
26
Apoptosis and Blebs
Outpouching of structure filled with blood or air Can get bigger and explode - spontaneous pneumothorax - Taken care of normally with phagocytosis
27
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
29
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
30
Irreversible Cell Injury
- Lysosomes - lytic enzymes kill the cell from within | Cytoskeleton starts to thicken and become sclerotic (hard)
31
Hallmark for irreversible cell damage / cell death
A lot of Ca going into the cell
32
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
33
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)
34
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...
35
Patterns of Accumulation
Normal but excessive Abnormal - something that shouldn't be in the cells Pigments - melanin - sunburns, suntan, freckles...injurious to skin
36
Pigments
``` Communicate injury to the cell Melanin = thick suntan Hemosiderin = bruises Lipofuscin = Liver spots Bilirubin = jaundice ```
37
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
40
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)
42
Tissue Necrosis Includes
1. Nuuclear changes and fragmentation 2. Membrane rupture 3. Cessation of cell function
43
-lysis
Dissolution or decomposition | Autolysis (used in some treatments for wondcare), self digestion of tissue
44
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
45
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)
46
Liquefactive is most common in
Nervous tissue
47
Caseous
Both coagulative and liquefactive necrosis TB is example Also seen in fungal infections Starts to look like cheese in structures with spots
48
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
49
Gangrene
Visible Necrosis
50
Dry Gangrene
Ischemic or Coagulative
51
Wet Gangrene
Liquefactive
52
Gas Gangrene
Caused by clostridia bacteria | - huge production of gas
53
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

FS Exam 3 (10 decks)

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