Cellular Injury/Death II Flashcards
1
Q
Oxidative stress
A
=Increased production and decreased scavenging of reactive oxygen species
2
Q
Morphologic manifestations
A
- Degeneration
- -Cell swelling
- Intracellular accumulations
- -Fatty change
- -Glycogen accumulation
- Hyaline changes
- -Hyaline droplets
- -Amyloid
- -Fibrinoid change
- -Extracellular hyaline
- Extracellular alterations
- -Fatty infiltration
3
Q
Degeneration
A
- Deterioration: sinking from a higher to a lower level or type
- A worsening of physical or mental qualities
- A retrogressive pathologic change in cells or tissues, in consequence of which the functions may be impaired or destroyed; at some stages, the degenerative process is reversible, but usually necrosis results
- Ex: hydropic degeneration, fatty degeneration
4
Q
Morphologic alterations in cell injury
A
- Reversible injury
- -Generalized cell swelling (hypoxia is most often the ultimate cause of acute cell swelling, regardless of the initiating event; hypoxia –> ATP depletion –> influx of water)
- -Within limits, the cell can repair these derangements
- Irreversible injury
- -Persistent or excessive injury causes cells to pass the “point of no return” into irreversible injury and cell death
- -Different injurious stimuli may induce cell death by necrosis or apoptosis
5
Q
Acute cell swelling
A
- Also known as hydropic degeneration (influx of water)
- -Commonly used when cell swelling occurs in hepatocytes or renal tubular epithelium
- Also known as ballooning degeneration
- -Keratinocytes in the epidermis, lining epithelium of the rumen
- Cell swelling is NOT the same as hypertrophy (=cells bigger as they gain proteins, organelles, etc.)
6
Q
Fatty change
A
=Fatty degeneration = steatosis = lipidosis
- Abnormal accumulation of lipid or fatty acid within the cell
- Reversible change
- Seen mainly in tissues involved in fat metabolism (such as hepatocytes)
7
Q
Glycogen accumulation
A
- Common in liver, kidney, heart, and skeletal muscle cells
- Physiologic causes:
- -CHO storage, high in liver after meals
- -Abundant glycogen in liver (newborns)
- Pathologic: alterations in glucose metabolism
- -Diabetes mellitus
- –Hepatocytes highly permeable to glucose
- -Steroid hepatopathy
- –Glucocorticoids stimulate glycogenesis in liver
- -Glycogen storage disease
- –Defective enzyme deficiency
- –Lysosomal storage disease
8
Q
PAS stain with v. without diastase
A
With diastase:
=Enzyme that breaks down glycogen
-Positive for stain uptake indicates CHO present, NOT glycogen
-Negative for stain uptake indicates glycogen had been present or NO CHO
-Must be used to differentiate between hydropic degeneration and glycogen accumulation, as they can appear similar otherwise
Without diastase
-Positive for stain uptake indicates CHO present
-Negative for stain uptake indicates NO CHO present
9
Q
Hyaline change
A
- Hyaline refers to any substance that has a homogeneous, eosinophilic, glassy appearance
- Categorized based on the nature of the material and/or location
- -Hyaline droplets - intracellular
- -Amyloid - extracellular
- -Fibrinoid change - extracellular
- -Extracellular hyaline (scar tissue)
10
Q
Amyloid
A
- Chemically diverse groups of extracellular proteinaceous substance that appear histologically similar
- -Protein structure is a beta-pleated sheet
- -Hard to metabolize, non-functioning
- Microscopically, amyloid is an eosinophilic amorphous hyaline substance
- -Extracellular and compresses adjacent tissues
- -Congo Red stain: stains amyloid orange/red, and under polarized light, amyloid glows an apple green fluorescence
- Lugol’s iodine tests for starch –> turns blue
11
Q
Amyloidosis in animals
A
- Systemic amyloidosis
- -Reactive systemic - AA protein
- –Predominant type of amyloid in animals
- -Familial - AA protein
- –Seen in Abyssinian cats and Shar Pei dogs
- Localized amyloidosis
- -Endocrine amyloid in cats - amylin
- -Neoplasms
- -Nasal amyloidosis in horses (AL protein)
12
Q
Reactive systemic amyloidosis
A
- Historically called secondary amyloidosis because it was secondary to chronic inflammation
- Serum amyloid A is a normal acute phase protein
- Inflammation –> release of IL-1 and IL-6 by macrophages –> synthesis of SAA protein by hepatocytes –> distribution of SAA via serum albumin to certain locations –> proteolysis –> formation of beta-pleated sheets (misfolding) –> insoluble protein (amyloid) deposited in certain extracellular sites (cannot be metabolized)
13
Q
Fibrinoid change
A
- Sometimes referred to as fibrinoid necrosis
- Pathogenesis:
- -Ag-Ab complexes
- –Deposited in vessel wall
- –Activate complement
- –Necrosis
- -Direct damage to vessel wall
- Looks like fibrin (but its not)
14
Q
Extracellular hyaline
A
- Scar tissue
- Dense fibrous connective tissue that occurs in some locations
- Occurrence:
- -CT (old scars)
- -Corpora albicans
- -Sclerotic glomeruli
- -Bowman’s capsule
- Cause:
- -Ischemia
- -Chronic injury
- -Aging change
- Gross:
- -+/- visible smooth, white glossy, firm
- Histo: ??
- Sequalae
- -No effects
- -Change in elasticity may interfere with organ function
15
Q
Fatty infiltration
A
- Accumulation of fat in extracellular stromal tissue; accumulation of adipocytes in tissue in which they are not normally present
- Occurs in many organs (common in skeletal and cardiac muscle)
- Cause:
- -Associated atrophy (decreased cell numbers) or necrosis
- -Obesity (too many fatty deposits in the tissues)
- -Seen in aged animals
