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[OS 201] 4th Lecture Exam > Cell Adaptation > Flashcards

Cell Adaptation Flashcards

1
Q

What is Principle #1 of Cell Injury

A

Cellular responses to injury depends on type of injury, duration, and severity and on the cell’s nutritional and hormonal status, and metabolic needs

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2
Q

What is Principle #2 of Cell Injury

A

Cell function is lost far before biochemical and subsequently morphological manifestations of injury become detectable.

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3
Q

What are the last indications of cellular damage?

A

Morphological Changes

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4
Q

What is Principle #3 of Cell Injury

A

Cells are complex interconnected systems, and single local injuries can result in multiple secondary and tertiary effects.

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5
Q

What is Principle #4 of Cell Injury

A

Cell injury results from functional and biochemical abnormalities in one or more of several essential cellular components

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6
Q

What is Principle #5 of Cell Injury

A

Because many of the biochemical systems of the cell are inter-dependent, injury at one site typically causes secondary injury to other cellular processes

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7
Q

4 Most Vulnerable Targets of Cellular Injury

A
  1. Cell membrane
  2. Mitochondrial function: energy metabolism- aerobic respiration and ATP production
  3. Functional and structural proteins: protein synthesis, enzyme function
  4. Genetic integrity
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8
Q

General Mechanisms of Injury (5)

A 
ATP Depletion
Loss of Plasma Membrane Integrity
Loss of Ca2+ Homeostasis
Mitochondrial Damage
Oxygen Deficiency
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9
Q

2 Pathways to Produce ATP

A 
Oxidative phosphorylation of ADP
Glycolytic Pathway (In the absence of oxygen)
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10
Q

What kind of tissues have an advantage when ATP levels fall?

A

Tissues with greater glycolytic capacity (like the liver)

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11
Q

What can occur when the plasma membrane is damaged?

A

Permeable to sodium and water leading to lysis

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12
Q

What happens if Potassium leaks out the cell?

A

RMP is disrupted leading to impaired nerve and muscle function

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13
Q

What happens when lysosomes are injured?

A

Release of hydrolytic enzymes leading to auto-digestion of cellular proteins

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14
Q

What happens when the ER is damaged?

A

Protein synthesis and intracellular transports are disrupted

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15
Q

What are important for targets of injurious stimuli, including hypoxia and toxins?

A

Mitochondria

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16
Q

Mitochondria can be damaged by ↑ of cytosolic Ca2+ by:

A
  1. Oxidative Stress
  2. Breakdown of phospholipids through the phospholipase A2 and sphingomyelin pathways by lipid breakdown products derived there from, such as free fatty acids and ceramide
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17
Q

Mitochondrial damage results in a high conductance channel called? Where is it found?

A

Mitochondrial Permeability Transition

Inner Mitochondrial Membrane

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18
Q

What gets activated due to (+) cytosolic calcium?

A

Protein Kinases

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19
Q

What’s wrong with overactive protein kinases?

A

This leads to the activation of other enzymes such asphospholipases, ATPases, proteases, and endonucleases which attack and break down critical components of the cell (lipid membranes, ATP, cytoskeletal proteins, DNA).

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20
Q

What are free radicals?

A

Highly reactive atoms that are chemically unstable and readily react with other molecules

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21
Q

Source of Free Radicals? (4)

A

Cellular Metabolism
Enzymatic Metabolism of Exogenous Channels
Ionizing Radiation
Divalent Metals

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22
Q

[Free Radicals]

How do they come from Cellular Metabolism

A

Produced from redox reactions

  1. Oxidative phosphorylation from mitochondria
  2. Neutrophils in inflammation
  3. Reperfusion and other oxidases (Xanthine Oxidase)
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23
Q

[Free Radicals]

How do they come from Enzymatic Metabolism of Exogenous Chemicals?

A

Some metabolites of chemicals and drugs are highly reactive free radicals (CCl4)

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24
Q

[Free Radicals]

How do they come from Ionizing Radiation?

A

Can hydrolyze water into Hydroxyl (OH-) and Hydrogen free radicals

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25
[Free Radicals] How do they come from Divalent Metals?
Transition metals (Cu, Fe) accepts/donate free elctrons
26
Free Radical Neutralization occurs through? (5)
o Spontaneous decay o Action of superoxide dismutase (SOD): 2O2• + 2H = H2O2 + O2 o Action of glutathione (GSH): 2 OH• + 2GSH = H2O2 + GSSG o Action of catalase: 2H2O2 = O2 + H2O o Endogenous and exogenous vitamins E,A, C, Beta carotene
27
Where are the most important free radicals derived from? Examples? (2)
Oxygen Superoxide and Hydroxyl Ions
28
[Free Radicals] Explain what happens in Lipid Peroxidation of Membranes
Double bonds in polyunsaturated membrane lipids are vulnerable to attack and can degrade the structural integrity of the cell membrane
29
[Free Radicals] Explain what happens in Damage to Proteins
Free radicals can fragment the polypeptide chain or call cross-linking of sulfhydryl groups in proteins resulting in degradation or loss of activity
30
[Free Radicals] Explain what happens in DNA Damage
Free radicals react with thymine in nuclear and mitochondrial DNA to create single stranded breaks or abnormal cross-linking
31
Major Antioxidant Enzymes (6)
1. Superoxide Dismutase (SOD) 2. Catalase 3. Glutathione Peroxidase 4. GSH (Reduced Glutathione) 5. GSSG (Oxdized Glutathione) 6. NADPH
32
When happens when cell DNA is damaged (2)
Interferes with cell replication | Impairs synthesis of important structural and functional proteins
33
Causes of Cellular Injury (6)
``` Hypoxia/Anoxia Physical Agents Chemical Agents Biological Agents Immunologic Reactions Nutritional Imbalances ```
34
Define: Hypoxia
Oxygen deprivation of cells
35
Difference Hypoxia and Ischemia
Ischemia is lack of blood and not only oxygen is lacking but also metabolic substrates like glucose
36
Which is worse: Hypoxia or Ischemia
Ischemia
37
What cells are most susceptible to hypoxia
Neurons
38
Define: Reperfusion Damaged
Cells that are reversibly injured due to ischemia can be damaged by restoration of blood flow Not exactly sure why it is caused but maybe due to high concentrations of calcium or increased free radicals
39
How does heat damage a cell?
Increased cellular activity resulting in less oxygen
40
How does cold damage a cell?
Crystal formation or slowing of metabolic activities
41
Explain how each do damage 1. Ionizing Radiation 2. Non-Ionizing Radiation 3. UV Radiation
1. Radiation above UV Range causes damage due to direct contact with a molecule causing electron imbalance and free radical formation 2. Low energy below visible light range (Lasers, microwaves, ultrasound) where the energy cannot break bonds but causes atoms to rotate/become misaligned 3. UV Radiation causes thymine dimerization
42
Differentiate Direct Chemical Agents and Indirect-Acting ones
D: React directly with cellular components I: Itself harmless to cells but toxic when metabolized and converted to a toxic substance, require activation
43
How does Cyanide damage a cell?
Inactivates cytochrome oxidase, an enzyme required for aerobic respiration
44
How does Mercury damage a cell?
Binds to sulfhydryl groups of cell membrane and other proteins causing increased membrane permeability and inhibition of ATPase dependent transport
45
How does Acetominophen damage a cell?
Detoxification uses Glutathione and large amounts would deplete it causing lipid peroxidation and ultimately cell death
46
3 Changes that Assist in Recognition of Atroph
1. Smaller cells 2. Organ's Framework (Stroma) appear to be more prominent than tis functioning portion (Parenchyma) 3. Presence of pigments called Lipofuschin, which is a remnant of cellular organelles digested by lysosomes
47
Hypertrophy is a result of increased cell number/cell size?
Cell Size only
48
Cell Populations that Cannot Deivide (3)
Cardiac Muscles Skeletal Muscles Nervous System Neurons
49
Differentiate: 1. Aplasia 2. Hypoplasia 3. Hyperplasia 4. Metaplasia 5. Dysplasia
1. No growth 2. Incomplete growth 3. Increased rate of growth 4. Adaptive conversion between cell types in an adult "reprogramming" 5. Abnormal cell growth
50
Differentiate Dysplasia and Cancer
Dysplastic cells are not autonomous and they are reversible
51
Reversible Cell Damage is called? | Irreversible Cell Damage is called?
Degeneration | Necrosis
52
Cause of cellular degeneration?
Failure of a cell to adapt or inadequate adaptations
53
Types of Cellular Degeneration (4)
1. Cloudy Swelling 2. Fatty Change 3. Intracellular Accumulations 4. Pathologic Calcifications
54
Cause of Cloudy Swelling
Failure of Na-K ATP-ase resulting in Na entering cell and K leaving causing an osmotic gain of water
55
Cause of Fatty Change
Degeneration cells accumulate lipids in cytoplasm, they push the nucleus further outward
56
Where do you usually find Fatty Change damage?
Liver due to alcoholism
57
Cause of Intracellular Accumulation
When normal cellular constituents or products occur in excess
58
Exogenous Intracellular Accumulation: Example
Carbon Dust (Anthracosis)
59
Endogenous Intracellular Accumulation: Example (3)
Aging pigment in liver, heart, and neurons Hemosiderin: Found in lungs following congestive heart failure. Called Hemosiderosis when found in a number of tissues and organs Bilirubin: Jaundice
60
Two Types of Pathologic Calcifications
Dystrophic | Metastatic
61
Define: Dystrophic Calcification
Deposition of calcium and other minerals in injured tissue e.g. atherosoma in blood vessels, heart valves in elderly individuals, old tuberculosis lesions
62
Define: Metastatic Calcification
Calcium deposition in NORMAL tissues in hypercalcemic stress
63
3 Types of Cell Death
1. Necrosis 2. Apoptosis 3. Autolysis
64
Steps of Apoptosis
1. Nuclear chromatin condensation and fragmentation 2. Cytoplasmic budding 3. Phagocytosis of extruded apoptotic bodies

[OS 201] 4th Lecture Exam (5 decks)

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