Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

[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

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

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

What are the last indications of cellular damage?

A

Morphological Changes

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

General Mechanisms of Injury (5)

A 
ATP Depletion
Loss of Plasma Membrane Integrity
Loss of Ca2+ Homeostasis
Mitochondrial Damage
Oxygen Deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

2 Pathways to Produce ATP

A 
Oxidative phosphorylation of ADP
Glycolytic Pathway (In the absence of oxygen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Tissues with greater glycolytic capacity (like the liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can occur when the plasma membrane is damaged?

A

Permeable to sodium and water leading to lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens if Potassium leaks out the cell?

A

RMP is disrupted leading to impaired nerve and muscle function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens when lysosomes are injured?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens when the ER is damaged?

A

Protein synthesis and intracellular transports are disrupted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

Mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Mitochondrial Permeability Transition

Inner Mitochondrial Membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What gets activated due to (+) cytosolic calcium?

A

Protein Kinases

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

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

What are free radicals?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Source of Free Radicals? (4)

A

Cellular Metabolism
Enzymatic Metabolism of Exogenous Channels
Ionizing Radiation
Divalent Metals

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

[Free Radicals]

How do they come from Ionizing Radiation?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

[Free Radicals]

How do they come from Divalent Metals?

A

Transition metals (Cu, Fe) accepts/donate free elctrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Free Radical Neutralization occurs through? (5)

A

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
Q

Where are the most important free radicals derived from?

Examples? (2)

A

Oxygen

Superoxide and Hydroxyl Ions

28
Q

[Free Radicals]

Explain what happens in Lipid Peroxidation of Membranes

A

Double bonds in polyunsaturated membrane lipids are vulnerable to attack and can degrade the structural integrity of the cell membrane

29
Q

[Free Radicals]

Explain what happens in Damage to Proteins

A

Free radicals can fragment the polypeptide chain or call cross-linking of sulfhydryl groups in proteins resulting in degradation or loss of activity

30
Q

[Free Radicals]

Explain what happens in DNA Damage

A

Free radicals react with thymine in nuclear and mitochondrial DNA to create single stranded breaks or abnormal cross-linking

31
Q

Major Antioxidant Enzymes (6)

A
  1. Superoxide Dismutase (SOD)
  2. Catalase
  3. Glutathione Peroxidase
  4. GSH (Reduced Glutathione)
  5. GSSG (Oxdized Glutathione)
  6. NADPH
32
Q

When happens when cell DNA is damaged (2)

A

Interferes with cell replication

Impairs synthesis of important structural and functional proteins

33
Q

Causes of Cellular Injury (6)

A 
Hypoxia/Anoxia
Physical Agents
Chemical Agents
Biological Agents
Immunologic Reactions
Nutritional Imbalances
34
Q

Define: Hypoxia

A

Oxygen deprivation of cells

35
Q

Difference Hypoxia and Ischemia

A

Ischemia is lack of blood and not only oxygen is lacking but also metabolic substrates like glucose

36
Q

Which is worse: Hypoxia or Ischemia

A

Ischemia

37
Q

What cells are most susceptible to hypoxia

A

Neurons

38
Q

Define: Reperfusion Damaged

A

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
Q

How does heat damage a cell?

A

Increased cellular activity resulting in less oxygen

40
Q

How does cold damage a cell?

A

Crystal formation or slowing of metabolic activities

41
Q

Explain how each do damage

  1. Ionizing Radiation
  2. Non-Ionizing Radiation
  3. UV Radiation
A
  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
Q

Differentiate Direct Chemical Agents and Indirect-Acting ones

A

D: React directly with cellular components
I: Itself harmless to cells but toxic when metabolized and converted to a toxic substance, require activation

43
Q

How does Cyanide damage a cell?

A

Inactivates cytochrome oxidase, an enzyme required for aerobic respiration

44
Q

How does Mercury damage a cell?

A

Binds to sulfhydryl groups of cell membrane and other proteins causing increased membrane permeability and inhibition of ATPase dependent transport

45
Q

How does Acetominophen damage a cell?

A

Detoxification uses Glutathione and large amounts would deplete it causing lipid peroxidation and ultimately cell death

46
Q

3 Changes that Assist in Recognition of Atroph

A
  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
Q

Hypertrophy is a result of increased cell number/cell size?

A

Cell Size only

48
Q

Cell Populations that Cannot Deivide (3)

A

Cardiac Muscles
Skeletal Muscles
Nervous System Neurons

49
Q

Differentiate:

  1. Aplasia
  2. Hypoplasia
  3. Hyperplasia
  4. Metaplasia
  5. Dysplasia
A
  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
Q

Differentiate Dysplasia and Cancer

A

Dysplastic cells are not autonomous and they are reversible

51
Q

Reversible Cell Damage is called?

Irreversible Cell Damage is called?

A

Degeneration

Necrosis

52
Q

Cause of cellular degeneration?

A

Failure of a cell to adapt or inadequate adaptations

53
Q

Types of Cellular Degeneration (4)

A
  1. Cloudy Swelling
  2. Fatty Change
  3. Intracellular Accumulations
  4. Pathologic Calcifications
54
Q

Cause of Cloudy Swelling

A

Failure of Na-K ATP-ase resulting in Na entering cell and K leaving causing an osmotic gain of water

55
Q

Cause of Fatty Change

A

Degeneration cells accumulate lipids in cytoplasm, they push the nucleus further outward

56
Q

Where do you usually find Fatty Change damage?

A

Liver due to alcoholism

57
Q

Cause of Intracellular Accumulation

A

When normal cellular constituents or products occur in excess

58
Q

Exogenous Intracellular Accumulation: Example

A

Carbon Dust (Anthracosis)

59
Q

Endogenous Intracellular Accumulation: Example (3)

A

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
Q

Two Types of Pathologic Calcifications

A

Dystrophic

Metastatic

61
Q

Define: Dystrophic Calcification

A

Deposition of calcium and other minerals in injured tissue

e.g. atherosoma in blood vessels, heart
valves in elderly individuals, old tuberculosis
lesions

62
Q

Define: Metastatic Calcification

A

Calcium deposition in NORMAL tissues in hypercalcemic stress

63
Q

3 Types of Cell Death

A
  1. Necrosis
  2. Apoptosis
  3. Autolysis
64
Q

Steps of Apoptosis

A
  1. Nuclear chromatin condensation and fragmentation
  2. Cytoplasmic budding
  3. Phagocytosis of extruded apoptotic bodies

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions