CHAPTER 1

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• cellular responses to stress? adaptive response, reversible injury, irreversible injury, cell death
• Adaptation? a reversible change in cell's number, size & metabolic activity,
• Adaptive responses? hypertrophy, hyperplasia, atrophy, metaplasia
• hypertrophy? incr. in cell size, thus in incr. organ -- cells limited capacity to divide
• physiological hypertrophy? breast & uterus during pregnancy + muscles after workout
• pathological hypertrophy? cardiac enlargm. due to hypertension or aortic valve disease
• hyperplasia? controlled incr. of number of cells, thus enlargment of organ, occurs when cells hav ability to replicate
• physiologic hyperplasia? hormonal and compensatory
• physiologic hyperplasia - compensatory? hepatocyte after partial hepatectomy
• phys. hyperplasia - hormonal? female breast gland during pregnancy
• pathol. hyperplasia? endometrial & prostate due to disturbed hormonal balance, warts in HPV, CT in wound healing
• Atrophy? Shrinkage in the size of a cell, decreased protein synthesis, increased protein degradation (ubiquitin-proteasome way) and autophagy („self-eating”)
• physiologic atrophy? Loss of endocrine stimulation in menopause, aging ( disuse, inadequate nutrition)
• pathologic atrophy? Denervation after trauma, Dimnished blood supply in advanced atherosclerosis
• Metaplasia? one type of adult cell replaced by another from the same germ layer, often due to chronic irritation, persistant could lead to malignancy
• Cell structures most prone to injury? cel membrane, SER, mithochondria
• principal mech. of cell injury? depletion of ATP, react. 02 sepcies in mithoch., disturbance in calcium homeostasis (lead to apotosis), incr. permab. of membranes, damage of DNA
• Reversible injury moprhlogical changes? fatty change & cellular swelling
• cellular swelling? pallor, turgor, incr. weight of organ, vacuolar degenerations
• Fatty change? liid vacuoles in cytopl, imbalance in fat metabolism, seen in kidney -heart-liver
• Reversible injury? Structural and functional abnormalities that don’t typically progress to severe membrane or nuclear damage
• Irreversible cellular injury? Structural and functional abnormalities that don’t typically progress to severe membrane or nuclear damage
• Necrosis? loss of membrane integrity, leakage of cell conent, inflammation, eosinophilia, death cell replaced by myelin, calcification , karyohexis &-lysis, pyknosis,
• Karyolysis? fading of the chromatin
• pyknosis? nuclear shrinkage and increased basophilia
• Karryohexis? fragmentation of nucleus
• Coagulative necrosis? infracts- areas of ischemic necrosis, In all solid organs exept the brain, well preseverved tissue
• Liquevative necrosis? bacterial/fungal infections & hypoxic death of cells within nervous system, Tissue transformed into liquid viscous mass
• caseous necrosis? "cheese-like", tuberculosis, Distinctive inflammatory border, Fragmented cells, granular pink
• Fat necrosis? typical for acute pancreatisis, release of activated pancreatic lipases into peritoneal cavity, Fatty acids + calcium= soap formation/ dystrophic calcification
• Fibrinoid necrosis? complexes of antigens and antibodies are deposited in arteries’ walls
• Gangerous necrosis? Refers to coagulative necrosis involving multiple tissue layers, mainly of the lower leg
• Apoptosis? No inflammation, no calcification, programmed, membrane intact - both physiol. & pathol.
• Function of apoptosis? removed injured/altered cells, maintain constnt no. of repliating cell, defense mech.
• Bcl-2 protein function? controls permeability of mithochondria
• Pro-apoptotic Bax and Bac function? form channels in mitochondrial membrane
• Cytochrome C? leaks into cytosol and activates caspaze -9
• pigments carbon, lipofuscin, melanin, hemosiderin
• carbon as pigmen charct.? causes anthracosis
• Lipofuscin? brown pigment that accumulates mainly in heart, liver and brain
• Hemosiderin? hemoglobin-derived large aggregates of ferritin micelles (physiologically in bone marr
• Dystrophic calcification? occurs in dead/dying tissues, cause of organ dysfunction (e.g. heart valves), normal ca2+ levels,
• Metatstatic calcification? occurs in normal tissues, secondary to hypercalcemia,
• Cause of hypercalcemia in metastasis? incr. secr. of PTH, bone destruction, Vit. D disorders, renal failure
• Where does metastasis mostly occur? kidney, lung, gastric mucosa
• Extracellular accumulation of proteins: Hyalinosis, Amyloidosis
• from ciliated columnar epithelium → stratified squamous epithelium, better survival, protective mechanism is lost- mucosal secretion and ciliary clearance. It may predispose to malignant transformation of the epithelium. in thorax and bronchi of smoker
• : Squamous to columnar nonciliated mucinous epithelium under the influence of refluxed gastric acid. Columnar epithelium is much better at handling acid, so when acid comes from the stomach, the cells of lower esophagus change in order to better deal with acid. Barrett esophagus
• inflammation of skeletal m results in metaplastic production of bone in skeletal muscle. Mostly due to trauma to skeletal muscle. The bone adjacent to is normal so no osteosarcoma, and it grows adjacent to the bone not on the bone. Myositis ossificans
• inability to correct mitochondrial dysfunction, lack of oxygen phosphorylation and ATP. Characteristic for irreversible injury
• Prions (protein) affected, Abnormal folding of PrPSC, causes neuronal cell death Creutzfeld- Jacob disease
• deposition occurs in dead or dying tissue dystrophic calcification
• metastatic calcification deposition of calcium salts in normal tissue
• Dystrophic calcification is common in area of caseous necrosis

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