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2420 Pathology > Module 3 Cellular Stress > Flashcards

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
Q

Response to Cell Injury Determinants

A
  • Exposure time to stressor (acute/chronic)
  • Severity of stimulus
  • Rate of division
  • Protective mechanisms
  • Nutritional/metabolic state
  • Blood supply
26
Q

Mechanisms of Cell Injury

A
  • Mitochondria damage
  • Calcium into cell
  • Plasma membrane damage
  • Protein misfolding/DNA damage
27
Q

Mitochondria Damage

A
  • Reduction of ATP
  • Increase in reactive oxygen species
  • Damage to lipids, proteins, DNA
28
Q

Calcium Entry

A
  • Increase mitochondrial permeability
  • Activation of cellular enzymes
29
Q

Plama Membranę Damage

A
  • Loss of cellular components
30
Q

Lysosomal Membrane Damage

A
  • Lysosomal enzymes digest cellular components
31
Q

Protein Misfiling/DNA Damage

A
  • Pro-apoptotic proteins triggered
  • Imitate programmed cell death
  • Faulty checkpoint/repair mechanism
  • Damaged cells cause apoptosis (cancer)
32
Q

Reversible Cell Injuries

A
  • Hydropic swelling
  • Fatty change
33
Q

Hydropic Swelling Causes

A
  • Chemical/biological toxins
  • Viral/bacteria infections
  • Ischemia/hypoxia
  • Excessive heat/cold
34
Q

Hydropic Swelling Characteristics

A
  • Increase in cell volume
  • Large, pale, vacuolated cytoplasm
  • No change to nucleus
  • Mitochondria swell
  • Cisternae of ER dilate
  • Blebs form on plasma membrane
35
Q

Hydropic Swelling Mechanism

A
  • Impairment to ionic controls (Na+ concentrations)
  • Impair Na+/K+ plasma membrane pump
  • Increase Na+ accumulation
  • Increase water
  • Maintain isosmotic conditions
36
Q

Fatty Change (Steatosis)

A
  • Adaptation to cell stressors
  • Accumulation of triglycerides
37
Q

Fatty Change Causes

A
  • Increase delivery of fat to cell (diabetes/starvation)
  • Impairment of fat metabolism (alcoholism)
  • Decrease apolipoprotein synthesis
38
Q

Fatty Change Mechanism

A
  • Fat vacuoles throughout cytoplasm
  • Displace nucleus
39
Q

Fatty Change Locations

A
  • Liver emphasis
  • Heart
  • Kidney
  • Skeletal muscle
40
Q

Necrosis

A
  • Uncontrolled cell death
  • Injury response
41
Q

Necrosis Characteristics

A
  • Intense eosinophilia (pinkness) of cytoplasm
  • Pyknosis (shrinkage) of nucleus
  • Karyorrhexis (break up) nucleus
  • Karyolysis (dissolution) of nucleus
42
Q

Gangrenous Necrosis ‘Wet’

A
  • Coagulative necrosis of limb
  • Superimposed infection
  • Liquefactive component
43
Q

Coagulative Necrosis

A
  • Most common
  • All components of necrosis
  • Ghost cells (structural outline)
  • Ischemia of myocardial cells
44
Q

Liquefactive Necrosis

A
  • Loss of tissue architecture
  • Digestion of dead cells
  • Bacterial infection
  • Brain tissue death
  • CNS cells
45
Q

Fat Necrosis

A
  • Adipose tissue
  • Enzymes digest fat
  • Complexes with calcium
  • Form white deposits
  • Pancreatitis, breast tissue damage
46
Q

Caseous Necrosis

A
  • Soft, friable, cheesy material
  • Tuberculosis characteristic
47
Q

Necrosis Signs

A
  • Chromatin clumping
  • Organelle swelling
  • Membrane damage
48
Q

Apoptosis

A
  • Morphologic manifestation
  • Programmed cell death
  • Energy dependent
49
Q

Physiological Apoptosis

A
  • During embryogenesis (finger/toe shaping)
  • Involution of thymus during development
  • Endometrium during menstrual cycle
  • Removal of infected/damaged cell
50
Q

Pathological Apoptosis

A
  • Radiation injury
  • Cancer
51
Q

Apoptosis Mechanism

A
  • Nucleus collapses due to chromatin condensation/fragmentation
  • Cell shrinks
  • Cleaved into cytoplasmic buds (enclose organelles)
  • Phagocytosis of extruded apoptotic bodies
52
Q

Ischemia

A
  • Reduction/interruption of blood flow
  • Most common cell injury
  • Cause of coagulative necrosis
  • Injury tissue faster than hypoxia
53
Q

Anoxia & Ischemia

A
  • Reduced levels/absence of O2
  • With blood flow loss
  • Steps resulting in necrosis
54
Q

Anoxia Impairments

A
  • Decreased O2 damages mitochondria (ATP damage)
  • Impairs ability to pump ions & water
  • Accumulation of Na+
  • K+ diffuses out
  • Cellular swelling
55
Q

Reversible with Oxygen Restoration

A
  • Increased anaerobic glycolysis
  • Depletion of glycogen stores
  • Lactic acid buildup
  • Ribosomes detach from RER
  • Decreased protein synthesis
56
Q

No Oxygen Restored

A
  • Proteolytic enzymes release
  • Calcium increases
  • Enzyme systems attack skeletal proteins
57
Q

Leakage of Cell Proteins

A
  • Detecting tissue specific cell injury
  • Measure blood levels

2420 Pathology (13 decks)

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