Robbins Chapter 2 Morphology Flashcards
First manifestation of almost all forms of injury to cells
cellular swelling
Appearance when there is cell injury to many cells
pallor, increased turgor, increase in weight of organ
Nonlethal injury pattern- distended and pinched off vacuoles in cytoplasm
hydropic change or vacuolar degradation
Ultrastructural changes of reversible cell injury
plasma membrane alterations
mitochondrial changes
dilation of the ER
nuclear alterations
Plasma membrane alterations in ultrastructural changes of reversible injury
blebbing, blunting, loss of microvilli
Mitochondrial changes in ultrastructural changes of reversible injury
swelling, small amorphous densities
Dilation of ER in ultrastructural changes of reversible injury
detachment of polysomes, myelin figures
Nuclear Alterations in ultrastructural changes of reversible injury
disaggregation of granular and fibrillar element
Necrotic cell appearance on histo slide
increased eosinophilia in H and E stain due to loss of
cytoplasmic RNA
more glassy homogeneous appearance
myelin figures
Myelin figures
large, whorled phospholipid masses that replace dead cells
Characteristics of a necrotic cell
discontinuities in plasma and organelle membranes, dilation of mitochondria, large amorphous densities, myelin figures, debris, fluffy denatured proteins
Nuclear changes of necrotic cell (3)
karyolysis
pyknosis
karyorrhexis
Karyolysis
change the reflects loss of DNA due to enzymatic degradation by endonuclease
Pyknosis
nuclear shrinkage and increased basophilia
chromatin condenses into solid, shrunken basophilic mass
Kayorrhexis
pyknotic nucleus undergoes fragmentation
Coagulative necrosis
architecture of dead tissue is maintained
localized area of coagulative necrosis is called an infarct
Liquefactive necrosis
digestion of dead cells
turns tissue into liquid viscous mass
pus can be secreted which contains dead leukocytes
Gangrenous necrosis
limb that has lost blood supply and undergone necrosis
Caseous necrosis
tuberculous infection most commonly seen
friable white appearance
“cheese-like”
Granuloma on microscopic exam
caseous necrosis
structureless collection of fragmented or lysed cells
Fat necrosis
focal areas of fat destruction usually from pancreatic lipase
“chalky white” appearance from fatty acids combining with calcium
Fibrinoid necrosis
seen in immune reactions involving blood vessels
see immune complexes with antigen and antibodies
Necroptosis appearance
resembles necrosis morphologically
resembles apoptosis mechanistically as programmed
What triggers necroptosis
ligation of TNFR1
viral proteins of RNA and DNA viruses
What signals are used in necroptosis
RIP1 and RIP3
caspase independent
Function of RIP1 and RIP3
reduce mitochondrial ATP generation
produce ROS
permeabilize lysosomal membranes
cause cellular swelling and membrane damage (necrosis)
How does inflammation occur in necroptosis
by releasing the cellular contents of the cell
When does pyroptosis occur in a cell
when a cel is infected by a microbe
What is activated in pyroptosis
caspase 1 which cleaves the precursor of IL-1 to make IL-1 active
What caspases cause death of the infected cell in pyrotosis
1 and 11
What happens during autophagy
sequestration of cellular organelles into autophagic vacuoles (autophagosomes)
fuse with lysosomes
digest the enclosed material
What is autophagy
adaptive response that is enhanced during nutrient deprivation causing the cell to cannibalize itself to survive
What can occur with dysregulation of autophagy
disease- cancer, inflammatory bowel diseases, neurodegenerative diseases
What accumulates during abnormal deposition of lipids- fatty change
free triglycerides in cells from defective transport or excessive intake
What accumulates during abnormal deposition of lipids- cholesterol deposition
cholesterol from defective catabolism or excesseive takes
When is accumulation of cholesterol deposition seen
in macrophages and smooth muscle of vessel walls in atherosclerosis
What occurs during abnormal deposition of proteins
reabsorb proteins in kidney tubules
immunoglobulins in plasma cells
Where is deposition of glycogen seen?
in macrophages of patients with defect in lysosomal enzymes that break down glycogen
How does deposition of pigments occur?
through indigestible pigments - carbon lipofuscin or iron
What is lipofuscin?
breakdown product of lipid peroxidation
Dystrophic calcification
deposition of calcium at sites of cell injury and necrosis
Metastatic calcification
deposition of calcium in normal tissues caused by hypercalcemia
4 causes of cellular aging
accumulation of DNA damage
replicative senescence
defective protein homeostasis
nutrient sensing system
How does accumulation of DNA damage cause cellular aging?
defective DNA repair systems
caloric restriction activates DNA repair– prolongs aging
How does replicative senescence cause cellular aging?
reduced capacity of cells to divide secondary to progressive shortening of telomeres
How does defective protein homeostasis cause cellular aging?
impaired chaperone and proteasome functions
How does the nutrient sensing system cause cellular aging?
caloric restriction increases longevity
mediators may be reduced by IGF-1 signaling and increasing sirtuins
