Cell Adaptions And Injury Flashcards
What are the 5 types of cell adaptations?
Atrophy Hypertrophy Hyperplasia Metaplasia Dysplasia
Decrease in size/number of cells and their metabolic activity
Atrophy
What are causes of atrophy?
Decreased workload Denervation Decreased blood supply/oxygen Inadequate nutrition Loss of endocrine stimulation Aging
What is the difference between atrophy and hypoplasia
Atrophy: decrease in size and cell number
Hypoplasia: never achieves full size (incomplete development)
What is aplasia
Lack of development of an organ/tissue
Increased size of cells and their functions
Hypertrophy
What types of cells are you likely to see hypertrophy as a cell adaptation?
Cells with little replication
Cardiomyocyte, skeletal muscle, and neurons
How can cardiac cell adaptations lead to cell injury if the stress is not relieved?
Cardiac hypertrophy -> limit beyond which enlargement is able to cope with the increased burden ->Regressive changed–> cardiac failure
An increase in the number of cells of an organ
Hyperplasia
Hyperplasia occurs in what types of cells
Cells capable of replication
What is most commonly caused by excessive hormonal or growth factor stimulation ?
Pathologic hyperplasia
A change in phenotype of a differrentated cell
Metaplasia
Metaplasia is an cell adaption in response to ________________ and can result in what changes?
Chronic irritation
Decreased function or increase propensity for malignant transformation
Metaplasia is most often seen in what type of cells?
Epithelial cells
Abnormal development of cells
Dysplasia
Usually epithelial cells
What are the two types of reversible cell injury?
Cellular swelling Fatty changes (lipidosis)
What are the two types of irreversible cell injury/death
Apoptosis
Necrosis
What is hydro pic degeneration?
Acute cell swelling
What cells are highly vulnerable to hypoxia and cell swelling?
Cardiomyocytes Proximal renal tubule epithelium Hepatocytes Endothelium CNS neurons, oligodendrocytes, astrocytes
Early, sub-lethal manifestation of cell damage characterized by increased cell size and volume due to H2O overload
Acute cell swelling
What is the etiology of acute cell swelling
Loss of ionic and fluid homeostasis
- > failure of cell energy function
- > cell membrane damage
- > injury to enzymes regulating ion channels of membrane
What is the pathogenesis of acute cell swelling?
Hypoxia (injury) -> decreased ATP production -> Na into cell and K out of cell-> osmotic pressure increases -> water moves into cell -> rupture of ER to form vacuoles -> hydropic degeneration
A tissue that is swollen with round edges, pallor, and slightly heavy compared to normal is characteristic of what cellular change
Acute cell swelling
Acute cell swelling of the epidermis is also called?
Ballooning dengeneration
What is the histological appearance of cellular swelling
Water dilutes the cytoplasm = enlarged and pale cytoplasm
Increase eosinophilia
Nucleus in normal position
What ultrastructural charges occur in cellular swelling?
Plasma membrane alterations (blebbing)
Mitochondrial changes
Dilation of ER and detachment of polysomes
Nuclear alterations
What is the difference between hydropic change and hypertrophy? And how do you differentiate the lesions
Hydropic change- increased uptake water
Hypertrophy - enlargement of cell and increased organelles
Cannot differentate microscopically
Microscopically - hydropic change will have pale cytoplasm and vacuolation. Hypertrophy will be enlarged but, slight disarray but still eosinophilic .
What pigment provides evidence of previous cell injury?
Lipofuscin “wear and tear”
What is sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation?
Fatty change (lipidosis)
What are the major types of lipids that can accumulate in cells?
Triglycerides
Cholesterol
Phospholipids
Lipid- carbohydrate
What are the main causes of fatty change
Hypoxia, toxicity, metabolic disorders, and abnormal synthesis/utilization/mobilization of fat
What type of cell changes are characterized by diffuse yellow colour, edges bulging , soft, friable, greasy texture?
Fatty change
In what cases can hepatic lipidosis be a physiological response?
Late pregnancy- pregnancy toxemia
Heavy early lactation (ketosis)
What nutritional disorders can lead through hepatic lipidosis
Obesity
Protein-calorie malnutrition (impaired apolipoprotein synthesis)
Starvation (mobilization of triglycerides)
What endocrine diseases can cause hepatic lipidosis?
Diabetes mellitus (mobilization of triglycerides)
Feline fatty liver syndrome
Fat cow syndrome
What is the histological appearance of fatty change
Well-delineated, lipid- filled vacuoles in cytoplasm
May displace cell nucleus to periphery
What morphological changes are associated with irreversible cell injury
Severe swelling of mitochondria
Extensive damage to plasma membranes
Swelling of lysosomes
______________ occurs after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury
Necrosis
What two cellular processes lead to necrosis?
Denturation of proteins
Enzymatic digestion of the cell (autolysis or release of lysosome contents from WBC)
An organ that is soft, friable, and sharply demarcated by a zone of inflammation is under going ____________
Necrosis
What changes can be seen histologically in a necrotic cell?
Pyknosis/karyorrhexis/Karyolysis
Increase eosinophilia (denatured proteins)
Loosing basophilia (Loss of RNA)
Glassy homogenous (loss of glycogen particles)
Vacuolation and moth eaten appearance (enzyme-digested cytoplasm organelles)
Calcification
What are the 6 types of tissue necrosis?
Coagulative Liquefactive Gangrenous Caseous Fat Fibrinoid
What is the common cause of coagulative necrosis
Ischemia (
Can occur in all solid organs but the brain
How can necrosis be distinguished histologically form autolysis ?
Necrotic tissue has a sharp zone of inflammation. Autolysis will not have a clear line
On what timeframe are necrotic changes seen?
Ultrastructurally- less than 6hours
Histologically - 6-12hrs
Grossly- 24-48hrs
Histologically, coagulative necrosis should appear
Foci/ localized area of coagulative necrosis (pale nuceli and cells)- architecture of dead tissue is preserved
Rim of leukocytes (basophilic)
Congestion and hemorrhage
_____________ necrosis is when cells are digested and transformed into a viscous mass
Liquefactive necrosis
What types of cells does liquefactive necrosis occur in?
Tissues with high neutrophil recruitment and enzymatic release with digestion of tissue
Tissue with high lipid content
Focal bacteria or fungal infections
*typically in CNS)
What is leukoencephalomalacia
Necrosis of the white matter of the brain
What is leukomelomalacia
Necrosis of the white matter of the spinal cord
What is polioencephalomalacia
Necrosis of the grey matter of the brain
What is poliomyelomalacia
Necrosis of the grey matter of the spinal cord
What can cause leukoenephalomalacia in horses, chickens, or pigs
Ingestion of Fusarium verticilioides -> produce Fumosisn B1 toxin -> inhibits sphingolipid synthesis -> direct cellular toxicity
What is a abscess? Can abscesses occur in the brain
Pus surrounded by a fibrous capsule
Not in CNS - no fibrous CT
What are the two types of abscesses?
Septic : infection and release of enzymes from WBC and infectious agent (most common)
Sterile: nonliving irritants (eg dugs)
What is the histology of liquefactive necrosis
Loss of cellular detail Granular cells Eosinophilic and basophilic debris No tissue architecture preserved Many neutrophils
What are the two types of generous necrosis
Dry - no bacterial infection
Wet-bacterial infection; tissue is wet and liquefactive
Usually begins as coagulative necrosis due to ischemia
Friable and white area of necrosis
Caseous necrosis
Casenous necrosis is usually due to ?
Chronic infections
Eg mycobacterium/corynebacterium/fusobacterium and fungal infections
Necrotic debris are dead WBC
Histologically, caseous necrosis appears as??
Eosinophilic granular cell debris with a rim of inflammatory cells
No tissue architecture
Dystrophic calcification in center of lesion (basophilic)
What are the three types of fat necrosis ?
Enzymatic
Traumatic necrosis of fat
Necrosis of abdominal fat
Describe enzymatic fat necrosis in the pancreas
Action of activated pancreatic lipase in “escaped” pancreatic fluid
Free fatty acid and Ca2+ -> calcium soaps (saponificaiton)
=> white and chalky necrosis
Form of necrosis usually seen in immune reactions involving blood vessels
Fibrinoid necrosis
What occurs must occur for formation of fribinoid necrosis
Ag-Ab complexes are deposited in the walls of arteries
Immune complexes with fibrin are leaked out of vessels => bright eosinophilic stain
Pathway of cell death activated by intrinsic enzymes that degrade the cellular components
Apoptosis
Apoptotic bodies break into fragments called?
Apoptotic bonds
How does apoptosis differ from necrosis
Apoptosis is programmed cell death (necrosis is not)
Inflammation seen in necrosis and not in apoptosis
What are some physiological process where apoptosis is involved?
Ebryogenesis
Hormone-dependent involution of organs (thymus and uterus post parturition)
Cell deletion in proliferation
Deletion of auto reactive Tcells
What are pathological apoptotic processes
TNF or FasL
DNA damage
Accumulation of misfolded proteins
Cell injury eg viral
Pathologic atrophy eg. duct obstruction
What cell morphology is seen in apoptosis ?
Cell shrinkage with increased cytoplasmic density
Pyknosis - chromatin condensation
Blebbing and apoptotic bodies
Phagocytosis of apoptotic cells by adjacent healthy cells
How are apoptotic bodies/cells removed?
Bodies: express phospholipids or coated with Ab or complement proteins -> phagocytosed
Cells: secreted factors to recruit phagocytes and express thrombospondidn
What disorders can occur with too little apoptosis ?
Increased cell survival
P53 mutations -> neoplasia
Self-Ag relative lymphocytes
Failure to remove dead cells
=> autoimmune
What disorders can occur with too much apoptosis?
Excessive cell death
Neurodegenerative: lose specific neurons-> mutations and misfolded proteins
Ischemic injury
Death of virus infected cells
