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Cellular reaction to injury (Pathology) - Coggle Diagram
Cellular reaction to injury (Pathology)
Adaptation to environmental stress
Hyperplasia
increase in the size
of an organ or tissue caused by an
increase
in the
number of cells.
Hypertrophy
increase in the size
of an
organ
or
tissue
due to an
increase in the size of cells
Aplasia
failure
of cell production
Atrophy
decrease in the size of an organ or tissue and results from a decrease in the mass of preexisting cells
presence of autophagic granules
Metaplasia
replacement of one differentiated tissue by another
Osseous metaplasia
formation of new bone at sites of tissue injury
Cartilaginous metaplasia
Myeloid metaplasia
proliferation of hematopoietic
Ex;e liver and spleen.
Squamous metaplasia
replacement of columnar epithelium at the squamocolumnar junction of the cervix by squamous epithelium
Ex;respiratory epitheliumof the bronchus,endometrium,pancreatic ducts.
Hypoplasia
decrease in cell production that is less extreme than in aplasia.
Turner syndrome and Klinefelter syndrome.
Hypoxic cell injury
cause
Ischemia
most common
Anemia
Carbon monoxide poisoning
Carbon monoxide poisoning
Poor oxygenation of blood
stage
Early stage
decreased ATP availability
Failure of the cell membrane pump
Swelling of the endoplasmic reticulum
Swelling of the mitochondria
Hydropic change
Disaggregation of ribosomes leads to failure of protein synthesis
Stimulation of phosphofructokinase activity
Late stage
membrane damage
loss of membrane phospholipids
Reversible morphologic signs of damage
formation
Myelin figures
Cell blebs
Cell death
Intracellular enzymes and various other proteins are released
Myocardial enzymes in serum.
Lactate dehydrogenase (LDH)
Creatine kinase (CK)
Aspartate aminotransferase (AST)
Troponins
troponin I and troponin T
myoglobin
Liver enzymes in serum.
AST
Alanine aminotransferase
Alkaline phosphatase
γ-glutamyltransferase
point of no return
irreversible damage to cell membrane
massive calcium influx, extensive calcification of the mitochondria
vulnerability of cells to hypoxic injury varies
Hypoxic injury becomes irreversible after
Three to 5 minutes for neurons
One to 2 hours for myocardial cells and hepatocytes
Many hours for skeletal muscle cells
Free radical injury
Meaning
molecules have a single unpaired electron in the outer orbital
Ex; superoxide O2 and e hydroxyl (OH• ) radicals
Mechanisms that generate free radicals
Normal metabolism
Oxygen toxicity
Ionizing radiation
Ultraviolet light
Drugs and chemicals
Reperfusion after ischemic injury
Mechanisms that degrade free radicals
Intracellular enzymes
Exogenous and endogenous antioxidants
vitamin A, vitamin C, vitamin E,cysteine, glutathione, selenium, ceruloplasmin, and transferrin
Spontaneous decay
glutathione peroxidase
glutathione peroxidase, catalase, and superoxide dismutase
Chemical cell injury
Meaning
the model of liver cell membrane damage induced by carbon tetrachloride (CCl4)
processed by the P-450 system
highly reactive free radical CCl3
lipid peroxidation of intracellular membranes
Widespread injury including:
Disaggregation of ribosomes
decreased protein synthesis
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Plasma membrane damage
cellular swelling
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Necrosis
General considerations
one of two contrasting morphologic patterns of tissue death
degradative and inflammatory reactions after death
caused by injury
occurs within living organisms
Autolysis
degradative reactions in cells
Postmortem autolysis
Heterolysis
refers to cellular degradation by enzymes derived from sources extrinsic to the cell
Types of necrosis
Coagulative necrosis
preservation of tissue architecture
Increased cytoplasmic eosinophilia
Nuclear changes
Karyorrhexis
Karyolysis
Pyknosis
Disappearance of stainable nuclei
Liquefactive necrosis
Ischemic injury to the central nervous system (CNS)
Suppurative infections
Caseous necrosis
part of granulomatous inflammation
interaction of T lymphocytes
Tuberculosis is the leading cause
amorphous eosinophilic appearance
Gangrenous necrosis
infective heterolysis and consequent liquefactive necrosis
wet gangrene.
coagulative necrosis without liquefaction
dry gangrene
Fibrinoid necrosis
deposition of fibrin-like proteinaceous material in the arterial walls
associated with immune-mediated vascular damage
Fat necrosis
Traumatic fat necrosis
severe injury to tissue with high fat contentant
Enzymatic fat necrosis
acute hemorrhagic pancreatitis
soap formation
Apoptosis
General considerations
second morphologic pattern of tissue death
removal of cells with irreparable DNA damage
Morphologic features
Involution and shrinkage
Biochemical events
extrinsic pathway of initiation
mediated by cell surface receptors exemplified by FAS
intrinsic, or mitochondrial, pathway
initiated by the loss of stimulation by growth factors and other adverse stimuli
Cytotoxic T-cell activation
Activation of transglutaminases
Regulation of apoptosis
mediated by a number of genes and their products
Reversible cellular changes and accumulations
Accumulations of exogenous pigments
Pulmonary accumulations of carbon (anthracotic pigment), silica, and iron dust
Plumbism
lead poisoning
Argyria
silver poisoning
Accumulations of endogenous pigments
Melanin
Hyaline change
hematoxylin and eosin sections
Pathologic calcifications
Fatty change (fatty metamorphosis and steatosis)
General considerations
accumulation of intracellular parenchymal triglycerides
liver, heart, and kidney
Imbalance among the uptake, utilization, and secretion of fat
Increased transport of triglycerides or fatty acids
Decreased mobilization of fat from cells
Decreased use of fat by cells
Overproduction of fat in cells