Summary's Chapter 2 Flashcards
First there will be some questions/an overview on the summary of patterns of cell injury and cell death.
Okay (p31 -p41). I made this questions from the blue ‘summary’ boxes in the book.
What are characteristics of reversible cell injury?
Cell swelling, fatty change, plasma membrane blebbing and loss of microvilli, mitochondrial swelling, dilation of the ER, eosinophilia (resulting from decreased cytoplasmic RNA)
What is necrosis?
Accidental cell death manifested by increased cytoplasmic eosinophilia; nuclear shrinkage, fragmentation, and dissolution; breakdown of plasma membrane and organellar membranes; abundant myelin figures; leakage and enzymatic digestion of cellular contents
What are the morphologic types of tissue necrosis?
Under different conditions, necrosis in tissues may assume specific patterns: coagulative, liquefactive, gangrenous, caseous, fat, and fibrinoid.
What is apoptosis?
Regulated mechanism of cell death that serves to eliminate unwanted and irreparably damaged cells, with the least possible host reaction, characterized by enzymatic degradation of proteins and DNA, initiated by caspases; and by rapid recognition and removal of dead cells by phagocytes
By which two major pathways is apoptosis initiated?
• Mitochondrial (intrinsic) pathway is triggered by loss of
survival signals, DNA damage, and accumulation of misfolded proteins (ER stress); associated with leakage of proapoptotic proteins from mitochondrial membrane into the cytoplasm, where they trigger caspase activation; inhibited by anti-apoptotic members of the Bcl family, which are induced by survival signals including growth factors.
• Death receptor (extrinsic) pathway is responsible for elimination of self-reactive lymphocytes and damage by CTLs; is initiated by engagement of death receptors (members of the TNF receptor family) by ligands on adjacent cells.
What are two other unusual pathways of cell death?
Necroptosis (which, as the name implies, includes features of both necrosis and apoptosis and is regulated by particular signaling pathways) and pyroptosis, which can lead to the release of proinflammatory cytokines and may initiate apoptosis.
What is autophagy?
Autophagy is an adaptation to nutrient deprivation in which cells digest their own organelles and recycle them to provide energy and substrates. If the stress is too severe for the process to cope with it, it results in cell death by apoptosis.
Next will be some questions about the summary of ‘mechanisms of cell injury’
Okay (p41-48)
Different … events cause cell injury and death by diverse mechanisms.
initiating
Where do hypoxia and ischemia lead to?
Hypoxia and ischemia lead to ATP depletion and failure of many energy-dependent functions, resulting first in reversible injury and, if not corrected, in necrosis.
True/False: In ischemia-reperfusion injury, restoration of blood flow to an ischemic tissue exacerbates damage by increasing production of ROS and by inflammation.
True
Oxidative stress refers to ….
Accumulation of ROS, which can damage cellular lipids, proteins, and DNA, and is associated with numerous initiating causes.
Protein misfolding depletes essential proteins and, if the misfolded proteins accumulate within cells, results in ….
Apoptosis
DNA damage (e.g., by radiation) also can induce … if it is not repaired.
Apoptosis
… is associated with cell injury because of the damaging actions of the products of inflammatory leukocytes.
Inflammation
Now the summary of cellular adaptations to stress is discussed
Oki (p48-51)
What is hypertrophy? (including cause and type of cells)
Increased cell and organ SIZE, often in response to increased workload; induced by growth factors produced in response to mechanical stress or other stimuli; occurs in tissues incapable of cell division
What is hyperplasia?
Increased cell numbers in response to hormones and other growth factors; occurs in tissues whose cells are able to divide or contain abundant tissue stem cells
What is atrophy?
Decreased cell and organ size, as a result of decreased nutrient supply or disuse; associated with decreased synthesis of cellular building blocks and increased breakdown of cellular organelles and autophagy
What is metaplasia?
Change in phenotype of differentiated cells, often in response to chronic irritation, that makes cells better able to withstand the stress; usually induced by altered differentiation pathway of tissue stem cells; may result in reduced functions or increased propensity for malignant transformation
Now we discuss the summary of abnormal intracellular depositions and calcifications
Okay (p51-54)
Abnormal deposits of materials in cells and tissues are the result of …
Excessive intake or defective transport or catabolism.
What are the different depositions of materials in cells/tissues?
Depositions of lipids, proteins, glycogen, pigments
What are the two different depositions of lipids?
- Fatty change: accumulation of free triglycerides in cells, resulting from excessive intake or defective transport (often because of defects in synthesis of transport proteins); manifestation of reversible cell injury
- Cholesterol deposition: result of defective catabolism and excessive intake; seen in macrophages and smooth muscle cells of vessel walls in atherosclerosis
What is the deposition of proteins?
Reabsorbed proteins in kidney tubules; immunoglobulins in plasma cells
What is the deposition of glycogen?
In macrophages of patients with defects in lysosomal enzymes that break down glycogen (glycogen storage diseases)
What is the deposition of pigments?
Typically indigestible pigments, such as carbon, lipofuscin (breakdown product of lipid peroxidation), or iron (usually resulting from overload, as in hemosiderosis)
What are the two different pathologic calcifications?
- Dystrophic calcification
- Metastatic calcification
What is dystrophic calcification?
Deposition of calcium at sites of cell injury and necrosis
What is metastatic calcification?
Deposition of calcium in normal tissues, caused by hypercalcemia (usually a consequence of parathyroid hormone excess)
Finally, we will discuss the summary of cellular aging
Okay (p54-56)
Results from a combination of multiple, progressive cellular alterations, including…:
• Accumulation of DNA damage and mutations
• Replicative senescence: reduced capacity of cells to divide secondary to progressive shortening of chromosomal ends
(telomeres)
• Defective protein homeostasis: loss of normal proteins and
accumulation of misfolded proteins
• Aging is exacerbated by chronic diseases, especially those associated with prolonged inflammation, and by stress, and is slowed down by calorie restriction and exercise.
