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

Cell Injury, Adaptation And Death Flashcards

Lectures 28 & 29 - Exam 4 (70 cards)

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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
What are the 2 general causes of oxygen deprivation?
hypoxia - oxygen deficiency ischemia - loss of oxygenated blood supply to tissues
26
What are some examples of chemical agents that can cause cell injury?
poisons, air pollutants, carbon monoxide, asbestos
27
What are some examples of infectious agents that can cause cell injury?
viruses, bacteria, fungi, parasites
28
What are some examples of immunological reactions that can cause cell injury?
autoimmune diseases
29
What are some examples of genetic defects that can cause cell injury?
sickle cell anemia, familial hypercholesterolemia
30
What are some examples of physical agents that can cause cell injury?
trauma, heat, cold, electric shock
31
What are some examples of nutritional imbalances that can cause cell injury?
- nutritional deficiencies (caloric or vitamin) - excess nutrition - diabetes (excess blood sugar levels) - atherosclerosis (can result in blockage of coronary arteries)
32
What causes cell injury during aging?
accumulation of damage by ROS loss of telomerase function
33
What are the two characteristics of reversible injury?
Cellular Swelling Fatty (acid) Changes
34
Define / describe cellular swelling
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
Define/describe fatty (acid) changes
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
What are the 2 characteristics of irreversible injury? What do they lead to?
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
What are the mechanisms of cell injury?
ATP depletion mitochondrial damage influx of calcium increased oxidative stress defects in membrane permeability
38
What is the mechanism of ATP depletion?
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
What is the mechanism of mitochondrial damage?
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
What are 2 ways to increase cytosolic Calcium concentration?
Release from the intracellular Calcium stores Calcium influx across the plasma membrane
41
What is the mechanism of injury when there is an influx of Calcium?
activation of various enzymes
42
What are the mechanisms of damage of oxygen-free radicals (OFRs) & ROS?
Lipid Peroxidation of membranes DNA fragmentation Proteins oxidation & cross-linking (C & M residues)
43
Describe the mechanism of "Lipid peroxidation of membranes"
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
Describe the mechanism of "DNA fragmentation"
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
Describe the mechanism of "Protein oxidation and cross-linking (C & M residues)"
Mechanism of cell injury by OFRs and ROS 1. Altered protein structure 2. Increased protein degradation 3. Loss of enzymatic activity
46
What are the 5 cellular mechanisms to deal with OFRs and ROS?
Superoxide Dismutase (SOD) Glutathione Peroxidase Catalase Antioxidants Sequestration of free ionized iron and copper
47
What is the reaction of Superoxide Dismutase (SOD)?
2 O2-. + 2 H+ -> H2O2 + O2
48
What is the reaction of Glutathione Peroxidase?
2 OH. + 2 GSH -> 2 H2O + G-S-S-G
49
What is the reaction of Catalase?
2 H2O2 -> 2 H2O + O2
50
Describe the role of antioxidants. Also list the classic examples.
to try to maintain a free radical balance by: - scavenging (reacting w/ & neutralizing) free radicals examples include Vitamin C and E & beta carotene
51
Describe the role of "Sequestration of free ionized iron and copper". Also list the classic examples.
- 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
What is the mechanism of damage of defects in membrane permeability?
Once the defects become irreversible... - Mitochondrial membrane damage - Plasma membrane damage - Lysosomal membrane damage
53
What are the effects of mitochondrial membrane damage due to defects in membrane permeability?
decreased ATP production, leading to necrosis and apoptosis
54
What are the effects of mitochondrial membrane damage due to plasma membrane damage?
loss of osmotic balance, influx of fluids and ions as well as loss of cellular contents
55
What are the effects of mitochondrial membrane damage due to lysosomal membrane damage?
leakage of enzymes into the cytoplasm and activation of the acid hydrolases in the acidic intracellular pH of the injured cells.
56
Define apoptosis
"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
List the physiological causes of apoptosis
- 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
List the pathological causes of apoptosis
- 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
What are the two mechanisms of apoptosis?
- 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
What is the difference between apoptosis and necrosis?
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
What are the "central players" in apoptosis?
Bcl-2 family proteins
62
List the members of the Bcl-2 family of proteins that have a role in apoptosis
Bax, Bak, Bad Bcl-2, Bcl-x
63
Describe the roles of Bax, Bak, and Bad
"pro-apoptotic" proteins -> the gas pedals increase mitochondrial membrane permeability by forming a dimer and inserting into the mitochondrial membrane.
64
Describe the roles of Bcl-2 and Bcl-x
"anti-apoptotic" proteins -> the brakes bind Bax family proteins and inhibit their function
65
What is the role of Cytochrome C?
Plays a role in apoptosis it is released from the mitochondria and can activate caspase c to initiate the caspase cascade
66
What are the two types of caspases?
initiators (caspase 8 & 9) executioners (caspases 3 & 7)
67
What happens once caspases are activated?
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
How are "blebs" formed?
dying cells collapse into cytoplasmic buds and apoptotic bodies
69
Describe the phagocytosis of apoptotic bodies by macrophages
- Dead cells are cleared before they can release their cytoplasmic contents - Prevents triggering an inflammatory response - Nothing remains of dead cell
70
Proteins and caspases to know
slide 45 of hudmon lecture 1

Patho - Exam 4 (6 decks)

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