Cellular accumulations Flashcards
(27 cards)
what are lysosomal subcellular responses?
Lysosomal catabolism
- types-> primary and secondary (phagocytosis)
- lysosomal inclusions-> lipids not degraded and may accumulate
- debris-> residual bodies
- lipofuscin: undigested remnants of lipid peroxide-> occurs with cellular aging
- tattoos: carbon particles may persist
- lysosomal storage disease: abnormal accumulations
What is heterophagy?
lysosomal catabolism
- digestion of material from extracellular environment
- requires endocytosis/phagocytosis/pinocytosis
- endosomes/phagosomes fuse with lysosomes
- most common phagocytosis in cells
what is autophagy?
- digestion of cells own components
- autophagic vacuole formed from ribosome-free region of rough ER
- fuse with lysosomes or Golgi to form autophagolysosome
- remove damaged organelles
What is induction (hypertrophy) of SER
adaptive responses-drugs
barbiturates-> induction of P-450 cytochrome system
alcohol and insecticides
what are subcellular mitochondrial alterations that happen?
pathological alterations in number, size and shape
- associated with hypertrophy and atrophy
- abnormal shapes in some toxic syndrome
- mitochondrial myopathies
what are subcellular cytoskeletal abnormalities?
interference with function due to drugs or genetic defects has severe consequences
- accumulation of damaged cytoskeletal elements is characteristic of some disease processes
- Mallory bodies-> alcoholic halines in alcoholic liver disease
- Neurofibrillary tangles-> Alzheimers disease
what are intracellular accumulation?
fatty changes
calcifications
protein changes
accumulation of pigments
what is the fattty change that happens?
Occurrence: liver (most common) due to chemical interference of lipid packaging
- can also happen to myocardium, muscle, kidney
- associated disease: alcoholism, diabetes, CCL3 poisoning, Reye’s syndrome
Mechanism to fatty change?
- fatty acids transported from adipose tissue and diet to liver
- > intracellular triglycerides must be complexed with lipid acceptor proteins to form lipoproteins
- inhibitors of fatty acid metabolism-> caused by many substances and types of injury-> chronic alcohol intake, toxins such as CCL, acetaminophen
- dispersion of ribosomes or damage by free radicals/Ca causes decreased protein synthesis resulting in decreased synthesis of lipid acceptor protein, decreased extracellular lipid transport and intracellular accumulation of triglycerides
morphology of fatty changes
- gross lesions: greasy, yellow, enlarged liver, yellow
- Microscopic lesions: non-staining (H and E) intracytoplasmic vacuoles
- clear vacuoles may contain water, glycogen, fat or other substances: true in fixed tissue where the process of tissue preparation removes the contents of the vacuoles
- can identify whats in vacuoles by dyes: Oil Red O or Sudan black on frozen tissue
calcifications?
may be extracellular or intracellular
what are the two types of calcifications?
dystrophic: Ca deposition in necrotic tissue
metastatic: Ca in viable due to hypercalcemia
Metastatic calcification characteristics?
- Ca in viable tissue
- hypercalcemia-> hyperparathyroidism, Vit. D toxicosis, tumors associated with increased bone catabolism, multiple myeloma, renal failure (2nd hyperpara)
- distributed lesions in vessels, kidneys, lungs
Dystrophic calcification characteristics?
necrotic tissue
localized
nomplexing of calcium with lipid cellular debris
amorphous basophilic deposits
general features of protein accumulations
- non-specific eosinophilic accumulations-> may be inside or outside of cells
- may be glassy, granular, or fibrillar depending on type and nature of protein
- eosinophilic cytoplasmic deposits-> hyaline change
examples of protein accumulations
- ) proximal renal tubules: associated with large amounts of proteinuria, leakage of proteins in glomerular filtrate partial resorption by proximal tubules
- Mallory bodies (intermediate keratin filaments) - ) Alpha-1 antitrypsin deficiency (mis-folding of proteins)
- accumulation of plasma proteins in alveoli or walls of blood vessel due to blood vessels damage or hypertension
microscopic apperanace of glycogen
non-staining cytoplasmic vacuoles PAS or periodic Shiff stain associated with abnormal glucose/glycogen metabolism -diabetes mellitus -glycogen storage disease
different pigments
Anthracosis Lipofuscin melanin hemosiderin biliruben
Exogenous pigments
anthracosis: accumulation of carbon particles in macrophages of lung
- tattoo ink: dermal macrophages
Lipofuscin
wear and tear pigment (aging pigment)
composed of lipid + phospholipid products
derived from turnover of membranes
non-toxic-does not interfere with function
very prominent in heart in liver: aging patients, severe malnutrition, cachexia associated with cancer
microscopically: gold-brown, granular perinuclear in cytoplasm
Melanin
produced by melanocytes
taken up by adjacent basal cells in the epidermis
stimulated by UV light
protects dividing basal cells from damage secondary to UV light exposure
Hemosiderin
-breaks down product of hemoglobin by macrophages
-aggregates of ferritin granules
-microscopically: gold-brown, granular
Examples: bruising=localized hemosiderosis
-hemochromatosis: genetic disease resulting in extreme accumulation of hemosiderin, affects liver (cirrhosis), pancreas (diabetes), skin(bronze color), pituitary (hypopituitarism)
Bilirubin
dervied from non-iron component of hemolgobin
normally excreted in bile
icterus/jaundice-> accumulates in tissues
may be extracellular or intracellular
what make up clear vacuoles?
may contain water, glycogen, fat or other substances
- particularly true in fixed tissues where the process of tissue preparation removes the contents of the vacuoles
- can visualize by Oil Red O or Sudan black on frozen tissue
