CHAPTER 1

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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