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Disease & Defense > LEC 9 Cellular Adaptation to Injury > Flashcards

LEC 9 Cellular Adaptation to Injury Flashcards

1
Q

What are the 6 mechanisms of cell injury?

A
  • Mitochondrial damage
  • Cell membrane damage
  • DNA damage
  • Oxidative stress
  • Disturbance in calcium homeostasis
  • Endoplasmic reticulum (ER) stress

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2
Q

How does michochondrial damage occur?

A
  • Damaged by increases of calcium, reactive oxygen species (ROS), and oxygen deprivation
  • Leads to inadequate aerobic respiration

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3
Q

What are the consequences of mitochondrial damage?

A
  • ATP depletion
  • Formation of ROS
  • Irreversible damage to mitochondrial and lysosomal membranes

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4
Q

How does cell membrane damage lead to cell injury?

A

Leads to increased permeability and damage to mitochondrial, plasma, and lysosomal membranes

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5
Q

Mitochondrial membrane damage results in the opening of what?

What does this cause?

A

Opening of the mitochondrial permeability transition pore (PTP)

Decreased ATP & release of proteins that trigger cell death

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6
Q

How can DNA damage lead to cell injury?

A
  • Mutations that affect p53 (and thus interfere with its ability to arrest cell cycling or to induce apoptosis) are associated with cancer development
  • p53 arrests cells in G1 or activates DNA repair mechanisms
  • If these mechanisms fail, p53 triggers apoptosis via the mitochondrial pathway

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7
Q

How does oxidative stress lead to cell injury?

A

Accumulation of oxygen-derived free radicals (ROS) resulting in:
* Lipid peroxidation - membrane damage
* Protein modifications - breakdown, misfolding
* DNA Damage - mutations

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8
Q

What are the 3 most important free radicals?

A
  • H2O2 (hydrogen peroxide)
  • *OH (hydroxyl radical)
  • O2*- (superoxide anion)

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9
Q

How does a disturbance in calcium homeostasis lead to cell injury?

A
  • Cytosolic free Ca2+ is normally maintained at LOW concentrations (~0.1 μmol) compared with extracellular levels (~1.3mmol)
  • Most intracellular Ca2+ is sequestered in mitochondria and the ER
  • Results in mitochondrial damage (loss of ATP) and damage to plasma and nuclear membranes

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10
Q

How does ER stress lead to cell injury?

A
  • Accumulation of misfolded proteins in the ER activates adaptive mechanisms that help the cell to survive
  • UNFOLDED PROTEIN RESPONSE
  • If the cellular repair capacity is exceeded, overload triggers apoptosis

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11
Q

What are the 3 examples of cell injury?

A
  • Oxygen Deprivation (hypoxia & ischemia)
  • Ischemia-Reperfusion
  • Chemical (Toxic)

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12
Q

Differentiate b/w hypoxia and ischemia.

A
  • Hypoxia: Decreased oxygen, though blood flow is maintained; energy production by anaerobic glycolysis can continue
  • Ischemia: Results from hypoxia induced by reduced blood flow, most often due to a mechanical arterial obstruction; can also be due to decreased venous drainage. Stops aerobic and anaerobic metabolism.

Ischemia causes more rapid & severe cell & tissue injury

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13
Q

How does ischemic cell injury occur?

A
  • Functional and morphologic consequences of decreased intracellular ATP due to mitochondrial damage
  • Reversible
  • Continued ATP depletion leads to cell death

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14
Q

How does Ischemic-Reperfusion injury occur?

A
  • Restoration of blood flow to ischemic tissues can promote recovery of cells if they are reversibly injured
  • However, it can also paradoxically exacerbate cell injury and cause cell death
  • Consequently, reperfused tissues may sustain loss of viable cells in addition to those that are irreversibly damaged by the ischemia
  • Caused by: Free Radical Production resulting in Apoptosis and Necrosis

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15
Q

What areas in the body are susceptible to hypoxia/ichemia?

A
  • Brain: (ACA/MCA/PCA boundary areas; hippocampus & cerebellum). “watershed areas” - border zones, receive dual blood supply from most distal branches of 2 arteries but susceptible to ischemia in states of systemic hypoperfusion
  • Heart: (LV subendocardium) - “watershed area”
  • Kidney: (areas of medulla)
  • Liver: (area around central vein - “zone 3”)
  • Colon: (Splenic flexure, rectum - “watershed areas”)

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16
Q

What are the 2 ways that chemicals induce cell injury?

A
  1. Direct toxicity: the chemical combines with critical molecular components. Ex: mercuric chloride, cyanide
  2. Conversion to toxic metabolites: most toxic chemicals must be converted to reactive toxic metabolites in the liver, which then act on target molecules. Ex: acetaminophen, Carbon Tetrachloride

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17
Q

What are adaptations?

A

reversible functional and structural responses to changes in physiologic states and some pathologic stimuli

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18
Q

What are the 4 major types for cellular adaptive response?

A
  • Atrophy
  • Hypertrophy
  • Hyperplasia
  • Metaplasia

Slide 19

19
Q

What is atrophy?

A
  • Shrinkage in size of the cells by loss of cell substance
  • Decreased weight and size of tissue or organ
  • Cells may turn off non-essential functions, but they are still alive

Slide 20

20
Q

What are some physiologic causes of atrophy?

A
  • Thymus atrophy with age
  • Uterus atrophy after parturition

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21
Q

What are some pathological causes of atrophy?

A
  • Decreased workload - disuse atrophy
  • Loss of innervation - denervation atrophy
  • Diminished blood supply - chronic ischemia
  • Inadequate nutrition
  • Loss of endocrine strimulation
  • Pressure (mass effect) -atrophy of normal tissue adjacent to large tumor

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22
Q

What are the biochemical mechanisms within the cell that cause atrophy to happen?

A
  • Decreased protein synthesis
  • Increased protein degradation (ubiquitin-proteasome pathway)
  • Autophagy (cell eats itself from inside) - evolutionarily conserved survival mechanism; Lipofuscin granules–>brown atrophy

Slide 22

23
Q

The image below shows an example of what?

Where the red arrow is specifically.

Cardiac Muscle
A

Brown Atrophy

caused by lipofuscin pigment

Slide 23

24
Q

The image below shows an example of what?

Circled parts

Spinal muscle
A

Denervation Atrophy

Reduced size of the spinal muscle w/i the circles d/t denervation

25
Q

What is hypertrophy?

A
  • Increase in cell size (not number) resulting in increased organ or tissue size
  • Occurs in organs where cells have a limited capacity to divide
    (e.g. - cardiac and skeletal muscle; no new cells!)

Slide 25

26
Q

What is the mechanism for hypertrophy?

A

Increased synthesis of structural proteins

Slide 25

27
Q

What are some physiological causes of hypertrophy?

A
  • Massive growth of the uterus during pregnancy (hormone-driven)
  • Body builders (response to demand)

Slide 25

28
Q

What is the most common stimulus for hypertrophy of skeletal and cardiac muscle?

A

Increased workload

Slide 25

29
Q

What is an example of a pathological cause of hypertrophy?

A

Enlargement of heart in response to pressure overload, usually resulting from either hypertension or valvular disease

Slide 25

30
Q

What is the biochemical mechanism for hypertrophy?

A
  • mechanical sensors detect stress
  • sensors activate complex signaling pathways
  • signaling pathways stimulate increased production of growth factors and vasoactive agents
  • these in turn, activate transcription factors that increase the expression of genes that encode muscle proteins

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31
Q

Which signaling pathway is associated with physiological (excercise induced) hypertrophy?

A

Phosphoinositide 3-Kinase (PI3K)/AKT pathway

Slide 26

32
Q

Which signaling pathway is associated with pathological hypertrophy?

A

G-protein coupled receptor initiated pathways

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33
Q

What is hyperplasia?

A

Increase in the number of normal cells

Same type of cell as the original

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34
Q

What is the biochemical mechanism of hyperplasia?

A
  • Growth-factor driven proliferation of cells via mitosis and cell division
  • Mature cells
  • Increased output of new cells from tissue stem cells

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35
Q

What are some causes of hyperplasia?

A
  • Hormonal stimulation
  • Chronic irritation
  • Stimulating antibodies
  • Viral infections

Slide 33

36
Q

How can pathologic hyperplasia lead to malignant cancer?

A
  • Hyperplasia is normally controlled and can be regulated
  • If this regulation is messed up, then it can lead to malignant change

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37
Q

What is metaplasia?

A
  • Replacement of one adult cell type by another adult cell type (reversible)
  • Adaptive: New cell type is better able to withstand the adverse environmental change that initiated metaplasia

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38
Q

What are the types of metaplasia?

A
  • Glandular to squamous (MOST COMMON) - epithelial tissue
  • Squamous to glandular - epithelial tissue
  • Connective tissue - Mesenchymal tissue

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Disease & Defense (37 decks)

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