Module 3 Cellular Stress Flashcards

1
Q

Cellular Proliferation

A
  • DNA replication
  • Synthesis of cellular constituents
  • Equal division during mitosis
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2
Q

Warburg Effect

A
  • Increased uptake of glucose & glutamine
  • Increased glycolysis
  • Decreased oxidative phosphorylation
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3
Q

Cell Growth Factors

A
  • Cell cycle progression
  • Changes in cellular metabolism
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4
Q

Changes in Cellular Metabolism

A
  • Biosynthesis of membranes/organelles
  • Warburg effect
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5
Q

Stem Cells During Development

A
  • Rise to differentiated tissues
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6
Q

Stem Cells in Adults

A
  • Replace damaged cells
  • Maintain tissue populations
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7
Q

Embryonic Stem Cells

A
  • Totipotent
  • Inner cell mass of blastocyst
  • Limitless self-renewal capacity
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8
Q

Totipotent

A
  • Give rise to any cell type
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9
Q

Tissue Stem Cells

A
  • Admixed with differentiated cells in tissues
  • Only generate normal constituents of tissue cells
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10
Q

Common Cell Adaptations

A
  • Cell size
  • Cell number
  • Phenotype & cell organization
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11
Q

Hypertrophy

A
  • Increase size of existing cells
  • Increase protein synthesis
  • Physiological or pathological
  • Response to increase in functional demand
  • Hormonal stimulation
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12
Q

Hyperplasia

A
  • Increase number of cells
  • Caused by cell division
  • Occur with hypertrophy
  • Increased demand/hormonal
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13
Q

Metaplasia

A
  • Change into different cell type
  • Unsuitable environment
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14
Q

Dysplasia

A
  • Alteration of size/shape/organization within tissue
  • Metaplastic squamous epithelium
  • Respiratory tract & cervix
  • Potentially reversible (remove irritant)
  • Preneoplastic lesion
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15
Q

Atrophy

A
  • Decrease mass
  • Cell size shrinkage
  • Reduced demand
  • Diminished blood supply/nutrition
  • Steady state reached for smaller cells
  • Physiologic or pathologic
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16
Q

Vulnerable Cell Components

A
  • Cell membranes (homeostasis)
  • Mitochondria (ATP energy)
  • Protein synthetic machinery
  • Cellular DNA
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17
Q

Hypoxia

A
  • Oxygen deprivation
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18
Q

Physical Agents

A
  • Mechanical trauma
  • Extreme temperature
  • Radiation
  • Pressure change
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19
Q

Chemical Agents

A
  • Air pollutants
  • CO
  • Pesticides
  • Poisons
  • Toxins
  • Drugs
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20
Q

Biological/Infectious Agents

A
  • Microorganisms
  • Viral/bacteria infections
  • Biological toxins
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21
Q

Immunologic Reactions

A
  • Allergens
  • Autoimmune disease
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22
Q

Genetic Alterations

A
  • Single mutations
  • Chromosomal abnormalities
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23
Q

Nutrition Imbalances

A
  • Protein-calorie deficiencies
  • Nutritional excess
24
Q

Cellular Aging

A
  • Lead to cell injury
  • Loss of intrinsic repair mechanisms
  • Repeated healing & repair
25
Response to Cell Injury Determinants
- Exposure time to stressor (acute/chronic) - Severity of stimulus - Rate of division - Protective mechanisms - Nutritional/metabolic state - Blood supply
26
Mechanisms of Cell Injury
- Mitochondria damage - Calcium into cell - Plasma membrane damage - Protein misfolding/DNA damage
27
Mitochondria Damage
- Reduction of ATP - Increase in reactive oxygen species - Damage to lipids, proteins, DNA
28
Calcium Entry
- Increase mitochondrial permeability - Activation of cellular enzymes
29
Plama Membranę Damage
- Loss of cellular components
30
Lysosomal Membrane Damage
- Lysosomal enzymes digest cellular components
31
Protein Misfiling/DNA Damage
- Pro-apoptotic proteins triggered - Imitate programmed cell death - Faulty checkpoint/repair mechanism - Damaged cells cause apoptosis (cancer)
32
Reversible Cell Injuries
- Hydropic swelling - Fatty change
33
Hydropic Swelling Causes
- Chemical/biological toxins - Viral/bacteria infections - Ischemia/hypoxia - Excessive heat/cold
34
Hydropic Swelling Characteristics
- Increase in cell volume - Large, pale, vacuolated cytoplasm - No change to nucleus - Mitochondria swell - Cisternae of ER dilate - Blebs form on plasma membrane
35
Hydropic Swelling Mechanism
- Impairment to ionic controls (Na+ concentrations) - Impair Na+/K+ plasma membrane pump - Increase Na+ accumulation - Increase water - Maintain isosmotic conditions
36
Fatty Change (Steatosis)
- Adaptation to cell stressors - Accumulation of triglycerides
37
Fatty Change Causes
- Increase delivery of fat to cell (diabetes/starvation) - Impairment of fat metabolism (alcoholism) - Decrease apolipoprotein synthesis
38
Fatty Change Mechanism
- Fat vacuoles throughout cytoplasm - Displace nucleus
39
Fatty Change Locations
- Liver *emphasis* - Heart - Kidney - Skeletal muscle
40
Necrosis
- Uncontrolled cell death - Injury response
41
Necrosis Characteristics
- Intense eosinophilia (pinkness) of cytoplasm - Pyknosis (shrinkage) of nucleus - Karyorrhexis (break up) nucleus - Karyolysis (dissolution) of nucleus
42
Gangrenous Necrosis 'Wet'
- Coagulative necrosis of limb - Superimposed infection - Liquefactive component
43
Coagulative Necrosis
- Most common - All components of necrosis - Ghost cells (structural outline) - Ischemia of myocardial cells
44
Liquefactive Necrosis
- Loss of tissue architecture - Digestion of dead cells - Bacterial infection - Brain tissue death - CNS cells
45
Fat Necrosis
- Adipose tissue - Enzymes digest fat - Complexes with calcium - Form white deposits - Pancreatitis, breast tissue damage
46
Caseous Necrosis
- Soft, friable, cheesy material - Tuberculosis characteristic
47
Necrosis Signs
- Chromatin clumping - Organelle swelling - Membrane damage
48
Apoptosis
- Morphologic manifestation - Programmed cell death - Energy dependent
49
Physiological Apoptosis
- During embryogenesis (finger/toe shaping) - Involution of thymus during development - Endometrium during menstrual cycle - Removal of infected/damaged cell
50
Pathological Apoptosis
- Radiation injury - Cancer
51
Apoptosis Mechanism
- Nucleus collapses due to chromatin condensation/fragmentation - Cell shrinks - Cleaved into cytoplasmic buds (enclose organelles) - Phagocytosis of extruded apoptotic bodies
52
Ischemia
- Reduction/interruption of blood flow - Most common cell injury - Cause of coagulative necrosis - Injury tissue faster than hypoxia
53
Anoxia & Ischemia
- Reduced levels/absence of O2 - With blood flow loss - Steps resulting in necrosis
54
Anoxia Impairments
- Decreased O2 damages mitochondria (ATP damage) - Impairs ability to pump ions & water - Accumulation of Na+ - K+ diffuses out - Cellular swelling
55
Reversible with Oxygen Restoration
- Increased anaerobic glycolysis - Depletion of glycogen stores - Lactic acid buildup - Ribosomes detach from RER - Decreased protein synthesis
56
No Oxygen Restored
- Proteolytic enzymes release - Calcium increases - Enzyme systems attack skeletal proteins
57
Leakage of Cell Proteins
- Detecting tissue specific cell injury - Measure blood levels