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40 Cards in this Set
- Front
- Back
Hyperplasia - types
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Hormonal hyperplasia --> breast
Compensatory hyperplasia --> liver resection Pathological hyperplasia --> wound healling |
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Causes of atrophy
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Decreased workload
Loss of innervation Diminished blood supply Inadequate nutrition Loss of endocrine stimulation Aging |
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Cachexia
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Wasting syndrome - loss of body mass that can not be reversed nutritionally
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Autophagy
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Starved cell eats its own components
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Metaplasia definition + cause
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Reversible change - adult cell type is replaced with another
Genetic ´reprogramming´ of stem cells--> epithelial metaplasia - response to chronic inflammation |
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Ischemia of myocardial cells
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1 - 2 min - noncontractile
20-30 min - cell death |
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Reversible injury
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Cellular swelling
Fatty change |
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Morphology of necrosis
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Swelling of ER
Lysosome rupture Nuclear condensation Swelling of mitochondria Fragmentation of cell membrane and nucleus High eosinophilia, pink-due to decreased cytoplasmic RNA Myelin figures--> large phospholipid masses from damaged membrane Pyknosis--> nuclear shrinkage Karyorrhexis--> pyknotic nucleus undergo fragmentation |
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Coagulative necrosis
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High protein tissues, parenchymatous organ, firm structure.
- heart, liver, spleen, lung Red--> yellow colour *old myocardial infarction is therefore coloured yellow. |
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Liquefactive necrosis
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Digestion of cells due to bacterial or fungal infection.
-brain, fat tissue |
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Coagulative necrosis
- Gangrenous necrosis |
Involves multiple tissue layers, complicated by bacterial infection--> attreact leukocytes-> ´wet gangrene´
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Caseous necrosis
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Tuberculous infection
- center of granulomas. ´cheese-like´ Surrounded by ring of macrophages and giant cells(Langhans cells) |
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Fat necrosis
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Release of active pancreatic lipase into peritoneal cavity and pancreas--> acute pancreatits
- pancreatic enz. and lipases split TGesters, release FA. FA combine with Ca2+ -->saponification |
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Fibrinoid necrosis
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Arterial wall and CT are infiltrated by immune complexes, show characteristic of fibrin.
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Can atrophy be induced?
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Injection of thyroxinen will decrease the need of thyroid gland. It will shrink.
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Free radical cell injury
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Lipid peroxidation of membranes
Cross-linking of proteins DNA fragmentation |
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Removal of free radicals
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-Superoxide dismutase
-GSH peroxidase - ratio GSH vs GSSG reflects cells ability to oxidize free radicals -Catalase in peroxisomes -Vit A, E, C and beta-carotene |
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Mercury chloride poisoning - mechanisms
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Binds to sulfhydryl groups of cell membrane proteins --> inhibits ATP-dependent transport
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Carbon tetrachloride poisoning
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CCl4-->CCl3 (in liver) by CYP450
Cause phospholipid peroxidation - breakdown of ER -low hepatic protein synthesis -swelling of ER -low lipid export--> fatty liver End resulat can be Ca2+ influx and cell death. |
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Normal(non-pathological) Apoptosis
-causes |
Embryogenesis
Implantation Involution of hormone dependent tissue Maintain constant nr. of cells Self reactive lymphocyte elimination Cell death induced by Tcyt-cells |
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Pathologic Apoptosis
-causes |
DNA-damage
Accumulation of misfolded proteins Viral infections Atrophy in parenchymal cells |
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Two pathways of apoptosis
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Intrinsic-mitochondrial--> cytochrome C
Extrinsic-death receptor-->Fas-TNF-receptor |
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Atherosclerosis
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Smooth muscle cells and macrophages are filled with lipid vacuoles --> plaques
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Xanthomas
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Accumulation of intracellular cholesterol in hereditary and aquired hyperlipidemic syndromes.
-subepithelial CT of skin or tendons - arranged in clusters, foamlike |
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"Alcoholoc hyaline"
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Seen in alcoholic liver disease, accumulation of intracellular cytoskeletal proteins becasue of cell injury - ´Mallorys bodies´ or ´Mallorys hyaline´
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Russell bodies
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Accumulation of Immunoglobulins
-seen in nasal polyp slide |
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Glycogen accumulation
- cause |
Glucose mtb abnormality
-Diabetes Mellitus- accumulation of glycogen in renal tubular cells, cardiomyocytes, beta-cells in islets of Langerhan. |
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Pigments
-exogenous |
Exogenous: Carbon--> anthracosis, blacken lymph nodes and pulmonary parenchyma
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Pigments
-endogenous |
Lipofuscin- marker of past free radical injury(heart, liver, brain)
Melanin Hemosiderin- stain Prussian blue, (bone marrow, spleen, liver) Bruise formation Hemosiderosis-->systemic overload of iron. First liver, bone marrow, spleen, lymph node->->progressive overload of whole body. |
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Hemosiderosis
-cause |
High absorption of iron
-impaired utilisation -hemolytic anemias -transfusions *hereditary hemochromatosis |
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Dystrophic calcification
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*atheromas->advanced atherosclerosis
-formation of crystalline phoshate -dying cells has no Ca2+ regulation+phosphate=insoluble precipitate. |
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Metastatic calcification
- Hypercalcemia, causes |
1. increased PTH secretion due to tumour.
2. destruction of bone - Paget´s disease immobilization multiple myeloma leukemia skeletal metastases 3. Vit. D disorders-->intoxication-sarcoidosis(activated vit.D precipitate) 4. Renal failure ->phosphate retention->secondary hyperparathyroidism |
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Russell bodies
|
Accumulation of Immunoglobulins
-seen in nasal polyp slide |
|
Glycogen accumulation
- cause |
Glucose mtb abnormality
-Diabetes Mellitus- accumulation of glycogen in renal tubular cells, cardiomyocytes, beta-cells in islets of Langerhan. |
|
Pigments
-exogenous |
Exogenous: Carbon--> anthracosis, blacken lymph nodes and pulmonary parenchyma
|
|
Pigments
-endogenous |
Lipofuscin- marker of past free radical injury(heart, liver, brain)
Melanin Hemosiderin- stain Prussian blue, (bone marrow, spleen, liver) Bruise formation Hemosiderosis-->systemic overload of iron. First liver, bone marrow, spleen, lymph node->->progressive overload of whole body. |
|
Hemosiderosis
-cause |
High absorption of iron
-impaired utilisation -hemolytic anemias -transfusions *hereditary hemochromatosis |
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Dystrophic calcification
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1.Necrotic tissue
2.Tissues undergoing slow regeneration *atheromas->advanced atherosclerosis -formation of crystalline phoshate -dying cells has no Ca2+ regulation+phosphate=insoluble precipitate. *heart valves - stenosis |
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Metastatic calcification
- Hypercalcemia, causes |
1. increased PTH secretion due to tumour.
2. destruction of bone - Paget´s disease immobilization multiple myeloma leukemia skeletal metastases 3. Vit. D disorders-->intoxication-sarcoidosis(activated vit.D precipitate) 4. Renal failure ->phosphate retention->secondary hyperparathyroidism |
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Hemochromatosis
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Inherited defect on chromosome 6 resulting in uncontrolled absortion of iron. Systems becomes overloaded with iron.
1. pancreas - fibrosis 2. liver - cirrhosis 3. skin - around sweat glands 4. heart muscle 5. mesenteric lymph nodes |