Module 3 Cellular Stress Flashcards
1
Q
Cellular Proliferation
A
- DNA replication
- Synthesis of cellular constituents
- Equal division during mitosis
2
Q
Warburg Effect
A
- Increased uptake of glucose & glutamine
- Increased glycolysis
- Decreased oxidative phosphorylation
3
Q
Cell Growth Factors
A
- Cell cycle progression
- Changes in cellular metabolism
4
Q
Changes in Cellular Metabolism
A
- Biosynthesis of membranes/organelles
- Warburg effect
5
Q
Stem Cells During Development
A
- Rise to differentiated tissues
6
Q
Stem Cells in Adults
A
- Replace damaged cells
- Maintain tissue populations
7
Q
Embryonic Stem Cells
A
- Totipotent
- Inner cell mass of blastocyst
- Limitless self-renewal capacity
8
Q
Totipotent
A
- Give rise to any cell type
9
Q
Tissue Stem Cells
A
- Admixed with differentiated cells in tissues
- Only generate normal constituents of tissue cells
10
Q
Common Cell Adaptations
A
- Cell size
- Cell number
- Phenotype & cell organization
11
Q
Hypertrophy
A
- Increase size of existing cells
- Increase protein synthesis
- Physiological or pathological
- Response to increase in functional demand
- Hormonal stimulation
12
Q
Hyperplasia
A
- Increase number of cells
- Caused by cell division
- Occur with hypertrophy
- Increased demand/hormonal
13
Q
Metaplasia
A
- Change into different cell type
- Unsuitable environment
14
Q
Dysplasia
A
- Alteration of size/shape/organization within tissue
- Metaplastic squamous epithelium
- Respiratory tract & cervix
- Potentially reversible (remove irritant)
- Preneoplastic lesion
15
Q
Atrophy
A
- Decrease mass
- Cell size shrinkage
- Reduced demand
- Diminished blood supply/nutrition
- Steady state reached for smaller cells
- Physiologic or pathologic
16
Q
Vulnerable Cell Components
A
- Cell membranes (homeostasis)
- Mitochondria (ATP energy)
- Protein synthetic machinery
- Cellular DNA
17
Q
Hypoxia
A
- Oxygen deprivation
18
Q
Physical Agents
A
- Mechanical trauma
- Extreme temperature
- Radiation
- Pressure change
19
Q
Chemical Agents
A
- Air pollutants
- CO
- Pesticides
- Poisons
- Toxins
- Drugs
20
Q
Biological/Infectious Agents
A
- Microorganisms
- Viral/bacteria infections
- Biological toxins
21
Q
Immunologic Reactions
A
- Allergens
- Autoimmune disease
22
Q
Genetic Alterations
A
- Single mutations
- Chromosomal abnormalities
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
