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Patho - Exam 4 > Cell Injury, Adaptation And Death > Flashcards

Cell Injury, Adaptation And Death Flashcards

Lectures 28 & 29 - Exam 4

1
Q

What is cell characteristic is affected during hypertrophy? How is the characteristic affected?

A

Affected: Size
How: increase in size (cell gets bigger)
“an increase in cell size resulting in an increase in the size of the organ”

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2
Q

Define adaptation (for cells)

A

As cells encounter physiological stresses or pathological stimuli, they can undergo adaptation, achieving a new steady state and preserving viability and function by changing their size, number, and form

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3
Q

Define cell injury

A

What occurs when cells are stressed to the point that they are unable to adapt

cells adapt -> too much stress -> cell injury

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4
Q

What are the 5 types of cell adaption?

A

hypertrophy
atrophy
hyperplasia
metaplasia
dysplasia

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5
Q

What cell types does hypertrophy affect?

A

cells that are incapable of dividing: striated muscle cells in both the skeletal muscle and the heart

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6
Q

What are some common causes of hypertrophy?

A

Increased workload - physiological stimuli
(ex - estrogen-induced uterus enlargement during pregnancy)
Pathological conditions
(ex - hypertension, MI)

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7
Q

Hypertrophy is characterized by….
(also list triggers)

A

Hypertrophy is characterized by… increased protein synthesis (graded increase of gene expression)
- Mechanical triggers such as stretching
- Hormonal triggers like adrenergic hormones

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8
Q

What is cell characteristic is affected during hyperplasia? How is the characteristic affected?

A

Affected: cell number
How: increase in number of cells

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9
Q

What are some common physiological cause(s) of hyperplasia?

A

Hormonal hyperplasia
- proliferation of the female mammary epithelium during puberty
Proliferation of connective tissue cells during wound healing (cuts, scrapes)
Physiologic compensatory hyperplasia
- regeneration of a partially resected liver by remaining hepatocytes (liver cells)

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10
Q

What are some common pathological cause(s) of hypertrophy?

A

Excessive hormonal or growth factor stimulation

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11
Q

What is cell characteristic is affected during atrophy? How is the characteristic affected?

A

Affected: cell size
How: decrease in cell size
“a shrinkage in the size of the cell by the loss of cell substance”

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12
Q

What are general causes of atrophy?

A

decreased workload
loss of inervantion
reduced blood supply
inadequate nutrition
aging (senile atrophy)

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13
Q

What causes a decrease in cell size?

A

increased cell atrophy or reduced protein synthesis

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14
Q

What is cell characteristic is affected during metaplasia? How is the characteristic affected?

A

Affected: cell type
How: reprogramming of stem cells to produce a different cell type

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15
Q

Is metaplasia reversible or irreversible?

A

metaplasia has a high chance of reversibility
(is reversible until it’s not)

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16
Q

What is/are common causes(s) of metaplasia?

A

metaplasia is often a response to chronic irritation and inflammation (triggered by the environment)
- response makes cells better able to withstand the stress

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17
Q

What are some examples of metaplasia?

A
  • In smokers, ciliated columnar cells are replaced by squamous epithelial cells, which are more rugged but not ciliated which leads to coughing and an increase in infections
  • barrett’s esophagus (wider & higher esophageal sphincter)
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18
Q

What is metaplasia a precursor to?

A

malignancy
often noncancerous

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19
Q

What is cell characteristic is affected during dysplasia? How is the characteristic affected?

A

Affected: cell development
How: organization of cells

“dysplasia is characterized by deranged cell growth of a specific tissue that results in cells that vary in size, shape, number, and organization”

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20
Q

What type of tissue does dysplasia typically affect?

A

epithelial tissue

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21
Q

Is dysplasia reversible or irreversible?

A

dysplasia is reversible until transformation:
Irregular nuclear envelope and chromatin (cytological) also architectural reconstruction
- ALSO dysplasia has the potential to be reversible after the irritation cause has been removed

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22
Q

Where does dysplasia commonly occur?

A

dysplasia often occurs in:
metaplastic squamous epithelium in the respiratory tract & uterine cervix

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23
Q

What is dysplasia a precursor to?

A

may lead to cancer

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24
Q

What are the eight causes of cell injury?
(categories)

A

oxygen deprivation
chemical agents
infectious agents
immunological reactions
genetic defects
physical agents
nutritional imbalances
aging - ROS damage

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25
Q

What are the 2 general causes of oxygen deprivation?

A

hypoxia - oxygen deficiency
ischemia - loss of oxygenated blood supply to tissues

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26
Q

What are some examples of chemical agents that can cause cell injury?

A

poisons, air pollutants, carbon monoxide, asbestos

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27
Q

What are some examples of infectious agents that can cause cell injury?

A

viruses, bacteria, fungi, parasites

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28
Q

What are some examples of immunological reactions that can cause cell injury?

A

autoimmune diseases

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29
Q

What are some examples of genetic defects that can cause cell injury?

A

sickle cell anemia, familial hypercholesterolemia

30
Q

What are some examples of physical agents that can cause cell injury?

A

trauma, heat, cold, electric shock

31
Q

What are some examples of nutritional imbalances that can cause cell injury?

A
  • nutritional deficiencies (caloric or vitamin)
  • excess nutrition
  • diabetes (excess blood sugar levels)
  • atherosclerosis (can result in blockage of coronary arteries)
32
Q

What causes cell injury during aging?

A

accumulation of damage by ROS
loss of telomerase function

33
Q

What are the two characteristics of reversible injury?

A

Cellular Swelling
Fatty (acid) Changes

34
Q

Define / describe cellular swelling

A

a characteristic of reversible injury

Cause: failure of energy-dependent ion pumps in the plasma membrane

Effect: leads to an inability to maintain ionic and fluid homeostasis

35
Q

Define/describe fatty (acid) changes

A

a characteristic of reversible injury that usually occurs in cells involved in metabolism such as hepatocytes & myocardial cells

Cause: hypoxic injury & various forms of toxic or metabolic injury

Effect: appearance of small/large lipid vacuoles in the cytoplasm

36
Q

What are the 2 characteristics of irreversible injury? What do they lead to?

A

Inability to reverse mitochondrial dysfunction
- lack of oxidative phosphorylation & ATP generation (no longer producing energy)

Membrane dysfunction: profound disturbances in membrane function
- holes in the membrane (outside & inside no longer separated)

37
Q

What are the mechanisms of cell injury?

A

ATP depletion
mitochondrial damage
influx of calcium
increased oxidative stress
defects in membrane permeability

38
Q

What is the mechanism of ATP depletion?

A
  1. Ischemia
  2. Decrease in oxidative phosphorylation
  3. Decrease in ATP
    4-?…. lots of problems

Ultimately…
ER swelling, cellular swelling, loss of microvilli, blebs, clumping of nuclear chromatin, decrease in protein synthesis

39
Q

What is the mechanism of mitochondrial damage?

A
  1. Increased cytostolic Ca2+, ROS (oxidative stress), lipid peroxidation
  2. mitochondrial injury / dysfunction (decreased ATP production)

Fast injury (no time to trigger apoptosis) - necrosis
Slow injury, “sick” mitochondria - apoptosis

40
Q

What are 2 ways to increase cytosolic Calcium concentration?

A

Release from the intracellular Calcium stores
Calcium influx across the plasma membrane

41
Q

What is the mechanism of injury when there is an influx of Calcium?

A

activation of various enzymes

42
Q

What are the mechanisms of damage of oxygen-free radicals (OFRs) & ROS?

A

Lipid Peroxidation of membranes
DNA fragmentation
Proteins oxidation & cross-linking (C & M residues)

43
Q

Describe the mechanism of “Lipid peroxidation of membranes”

A

Mechanism of cell injury by OFRs and ROS

  1. Carbon-carbon double bonds are attacked
  2. Peroxidated membrane lipids are less hydrophobic
  3. Loss of hydrophobicity converts the lipids to detergents
  4. Membrane integrity is reduced
44
Q

Describe the mechanism of “DNA fragmentation”

A

Mechanism of cell injury by OFRs and ROS

  1. Thymine (per)oxidation: base pairing between T and A is altered, leading to repair featuring mis-substitution (mutation)
  2. Single-stranded DNA breaks: breakage of phosphodiester backbone
    reduced replication and transcription
45
Q

Describe the mechanism of “Protein oxidation and cross-linking (C & M residues)”

A

Mechanism of cell injury by OFRs and ROS

  1. Altered protein structure
  2. Increased protein degradation
  3. Loss of enzymatic activity
46
Q

What are the 5 cellular mechanisms to deal with OFRs and ROS?

A

Superoxide Dismutase (SOD)
Glutathione Peroxidase
Catalase
Antioxidants
Sequestration of free ionized iron and copper

47
Q

What is the reaction of Superoxide Dismutase (SOD)?

A

2 O2-. + 2 H+ -> H2O2 + O2

48
Q

What is the reaction of Glutathione Peroxidase?

A

2 OH. + 2 GSH -> 2 H2O + G-S-S-G

49
Q

What is the reaction of Catalase?

A

2 H2O2 -> 2 H2O + O2

50
Q

Describe the role of antioxidants. Also list the classic examples.

A

to try to maintain a free radical balance by:
- scavenging (reacting w/ & neutralizing) free radicals
examples include Vitamin C and E & beta
carotene

51
Q

Describe the role of “Sequestration of free ionized iron and copper”. Also list the classic examples.

A
  • Free ionized iron and copper can cause ROS and oxygen free radical production via Fenton reaction, they sequester the metal ions & prevent them from causing ROS/OFR production

EXAMPLES: Transferrin (Fe), ferritin (Fe), and ceruloplasmin (Cu)

52
Q

What is the mechanism of damage of defects in membrane permeability?

A

Once the defects become irreversible…

  • Mitochondrial membrane damage
  • Plasma membrane damage
  • Lysosomal membrane damage
53
Q

What are the effects of mitochondrial membrane damage due to defects in membrane permeability?

A

decreased ATP production, leading to necrosis and apoptosis

54
Q

What are the effects of mitochondrial membrane damage due to plasma membrane damage?

A

loss of osmotic balance, influx of fluids and ions as well as loss of cellular contents

55
Q

What are the effects of mitochondrial membrane damage due to lysosomal membrane damage?

A

leakage of enzymes into the cytoplasm and activation of the acid hydrolases in the acidic
intracellular pH of the injured cells.

56
Q

Define apoptosis

A

“Apoptosis is a pathway of cell death that is induced by a tightly regulated suicide program in which cells destined to die activate enzymes capable of degrading the cells’ own nuclear DNA and cytoplasmic proteins.”

57
Q

List the physiological causes of apoptosis

A
  • Programmed destruction of cells during embryogenesis
  • Involution of Hormone-dependent tissues upon hormone deprivation (ex = endometrial cell breakdown during the menstrual cycle)
  • Cell loss in proliferating cell populations (ex = intestinal crypt epithelia)
  • Elimination of potentially harmful self-reactive lymphocytes: before or after their maturation
  • Cell death induced by cytotoxic T lymphocytes
58
Q

List the pathological causes of apoptosis

A
  • DNA damage
  • accumulation of misfolded proteins
  • cell injury in certain infection (viral infections)
  • pathological atrophy in parenchymal organs after duct obstruction (pancreas, kidney and parotid gland)
59
Q

What are the two mechanisms of apoptosis?

A
  • Mitochondrial Pathway / Intrinsic Pathway
    induced w/in the cell, sensors inside the cell make the decision
  • Death Receptor Pathway / Extrinsic Pathway
    induced by something outside the cell
    ex = cytotoxic T-cells
60
Q

What is the difference between apoptosis and necrosis?

A

apoptosis is PROGRAMMED, necrosis is not
apoptotic cells are consumed by phagocytes before their cytoplasmic contents are released and an inflammatory response is triggered

61
Q

What are the “central players” in apoptosis?

A

Bcl-2 family proteins

62
Q

List the members of the Bcl-2 family of proteins that have a role in apoptosis

A

Bax, Bak, Bad
Bcl-2, Bcl-x

63
Q

Describe the roles of Bax, Bak, and Bad

A

“pro-apoptotic” proteins -> the gas pedals
increase mitochondrial membrane
permeability by forming a dimer and inserting into the mitochondrial membrane.

64
Q

Describe the roles of Bcl-2 and Bcl-x

A

“anti-apoptotic” proteins -> the brakes
bind Bax family proteins and inhibit their function

65
Q

What is the role of Cytochrome C?

A

Plays a role in apoptosis
it is released from the mitochondria and can activate caspase c to initiate the caspase cascade

66
Q

What are the two types of caspases?

A

initiators (caspase 8 & 9)
executioners (caspases 3 & 7)

67
Q

What happens once caspases are activated?

A

Activated caspases can activate:
- other proteases, which causes a degradation of cytoskeletal proteins
- endonucleases, which causes cleavage of DNA leading to DNA fragmentation (DNA ladder)

68
Q

How are “blebs” formed?

A

dying cells collapse into cytoplasmic buds and
apoptotic bodies

69
Q

Describe the phagocytosis of apoptotic bodies by macrophages

A
  • Dead cells are cleared before they can release their cytoplasmic contents
  • Prevents triggering an inflammatory response
  • Nothing remains of dead cell
70
Q

Proteins and caspases to know

A

slide 45 of hudmon lecture 1

Patho - Exam 4 (6 decks)

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