Cellular Adaptations and Death Flashcards
What are the mechanisms that can cause atrophy
Decreased protein synthesis
Increased protein degradation
What is the most common cause for hypertrophy
Increased workload
(skeletal muscles, uterus, heart)
What causes an increase in the production of cellular proteins
mechanical stretch (more work)
Agonists (hormones, enzymes)
GFs
What causes differentiation in metaplasia
Cytokines, GF, ECM signaling alter gene expression and lead to differentiation
What are the general causes of cell injury
Hypoxia
Physical damage
Chemical damage
Infection
Immune reactions
Genetic derangement
Nutritional imbalances
What does the response to cell unjury depend on
The nature, duration, and severity of the injury
reversible injury - cell membrane
Blebbing
Distirtion
reversible injury - ER
detachment of ribosomes
reversible injury - mitochondria
amorphous densities
reversible injury - lysozomes
Autophagy
reversible injury - nuclei
chromatin clumping
reversible injury - gross appearance
Pallor
Swelling
Increased weight
organ-opathy
reversible injury - histo
Hydropic degeneration
Increased cell volume
Cytoplasm vacuolization
Peripheral nuclei
Apoptsis:
Carefully regulated cell death
What are the apoptotic pathways
Intrinsic and extrinsic
What triggers the intrinsic pathway
Loss of stimulation or GFs
What triggers the extrinsic pathway
Death receptors
What do both apoptotic pathways result in (not the end result - where the pathways merge)
Executioner caspase activation
Apoptosis - ultrastructure
Cell shrinkage
Condensation of nuclear chromatin and cytoplasm
Cytoplasmic blebs
Apoptotic bodies
Apoptosis - histo
Single cells or small clusters
Round or oval, intensely eosinophilic cytoplasm
Dense nuclear chromatin
Minimal inflammation
Can necrosis be physiologic
No
Necrosis - mechanism
Permanent mitochondrial damage
Severe disturbance in membrane function
Ca influx –> activates phospholipase A
Necrosis - cell membrane
Defects, myelin figures
Necrosis - ER
Lysis, loss of ribosomes
Necrosis - mitochondria
Large, amorphous densities
Necrosis - lysosomes
rupture, release of enzymes
Necrosis - nuclei
Pyknosis, karyorrhexis, karyolysis
Pyknosis:
Nucleus is small and dense
Karyorrhexis
Nucleus is in little fragments
Karyolysis
Nucleus fades and disappears
What are the main necrosis morphologies
Coagulative
Liquefactive
Caseous
Coagulative necrosis - what happens
Enzymes denature tissues
Structural outline is preserved
coagulative necrosis - where does it happen
Any tissue except the brain
coagulative necrosis - causes
Hypoxia, ischemia, acute toxicity, thermal injuries
coagulative necrosis - gross
grey, white, yellow, or red
Depressed
Soft
coagulative necrosis - histo
Tissue architecture preserved
Homogenous eosinophilic area
Nuclear change may or may not be present
Liquefactive necrosis - what happens
Enzymatic or cellular degradation of cellular components
Tissue architecture is not preserved
Liquefactive necrosis - where does it happen
Any tissue
ONLY type that occurs in the brain
Liquefactive necrosis - causes
Bacterial or fungal infection, severe burns, chemical injuries
Liquefactive necrosis - gross
Creamy, opaque material oozes from tissue
May or may not be encapsulated
Can be hard to distinguish from inflammation
Liquefactive necrosis - histo
Loss of recognizable tissue architecture and cellular details
Eosinophilic proteinaceous material
Cellular debris
Variabel amounts of inflammation (depends on cause)
Caseous necrosis - what is it
used to denote specific pathology
Pathogens induce a specific response in tissue
Caseous necrosis - gross
White, gray, yellow material
Thick, pasty, cheese-like
Dry, slightly greasy, firm
May be lamellated
May have areas of mineralization
Caseous necrosis - histo
Loss of recognizable tissue architecture and cellular details
Granulomatous and lymphocytic inflammation
Giant cells
May have mineralization
Malacia:
Necrosis of the CNS
Remember - brains only do liquefactive necrosis
What is another term for fat necrosis
Saponification
Main categories of saponification
Enzymatic
Non-enzymatic (trauma)
Dry gangrene:
Coagulative necrosis of an extremity
Dry gangrene - gross
Shrunken and leathery
Necrotic material may slough
Dry gangrene - clinically
Cold and dark color
Dry gangrene - histo
Coagulative necrosis
Small numbers of bacteria
Wet gangrene:
Liquefactive necrosis
Happens when necrotic tissue retains moisture and warmth
Superimposed bacterial infection
wet gangrene - gross
Wet, dark, may contain gas pockets
wet gangrene - histo
Liquifactive and coagulative necrosis, bacteria, gas bubbles
Apoptosis - overall cell morphology
Shrunken and convoluted
Necrosis - overall cell morphology
Swollen and disrupted