Cell Injury and Death Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cellular Aging

A

Loos of ability of a cell to divide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Stressor - Physical

A
Trauma
Temp extremes
Ionizing (chemo) radiation
Pressure (aquatic therapy)
Electrical energy
Mechanical energy (prolonged loud noises damage ear)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Stressor - Microorganisms

A
Bacteria
Viruses
Fungi
Parasites
They all have different role and produce different things
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Stressor - Nutritional/Metabolic Imbalances

A
  • Leads to dec. or impaired cellular function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Adaptation - Atrophy

A

Decrease or shrinkage in size of the cell

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Metaplasia

A
  • One adult cell type is replaced with another adult cell type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Most Common Metaplasia

A

Epithelial cells being replaced by mesenchymal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Metaplasia Examples

A

Respiratory Tract - smokers - columnar to epithelial

Muscle - muscle fibers ossify - abnormal

23
Q

Dysplasia

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

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
Q

Cell Necrosis

A

Cell Death
Injurious to tissue
Always pathological
Will produce inflammation

26
Q

Apoptosis and Blebs

A

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

27
Q

Necrosis and Blebs

A

Gets bigger and bigger and ruptures the cell

Some lytic agents might be released and then lead to inflammatory response

28
Q

Cellular Swelling

A
  • 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
Q

Fatty Changes

A
  • 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
Q

Irreversible Cell Injury

A
  • Lysosomes - lytic enzymes kill the cell from within

Cytoskeleton starts to thicken and become sclerotic (hard)

31
Q

Hallmark for irreversible cell damage / cell death

A

A lot of Ca going into the cell

32
Q

Irreversible Cell Changes

A
  • 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
Q

Cell Death

A
  • 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
Q

Accumulation Patterns of Cell Injury

A
  • Under certain conditions the cell will accumulate substances within the cytoplasm
  • These might be short or long term (more permanent)
  • Lipids, glycogen…
35
Q

Patterns of Accumulation

A

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

36
Q

Pigments

A
Communicate injury to the cell
Melanin = thick suntan
Hemosiderin = bruises
Lipofuscin = Liver spots
Bilirubin = jaundice
37
Q

Stages of a bruise

A
  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
Q

Caveat to stages of bruise

A

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
Q

PT and bruising

A

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
Q

Calcium

A
  • 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
Q

Tissue Necrosis

A
  • Refers to outcome of cell death
  • Only in living (dead = decay)
  • Autolysis action (requires autolytic activity within you)
42
Q

Tissue Necrosis Includes

A
  1. Nuuclear changes and fragmentation
  2. Membrane rupture
  3. Cessation of cell function
43
Q

-lysis

A

Dissolution or decomposition

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

44
Q

Coagulative Necrosis

A

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
Q

Liquefactive

A
  • 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
Q

Liquefactive is most common in

A

Nervous tissue

47
Q

Caseous

A

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

48
Q

Fat Necrosis

A
  • 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
Q

Gangrene

A

Visible Necrosis

50
Q

Dry Gangrene

A

Ischemic or Coagulative

51
Q

Wet Gangrene

A

Liquefactive

52
Q

Gas Gangrene

A

Caused by clostridia bacteria

- huge production of gas

53
Q

PT Gangrene

A

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