Regressive chnages: necrosis, apooptosis, involution, atropphy, dysplasia, autolysis Flashcards
rversible chnages
atrophy and dystrophy(lipid, proteins and saccharides)
irreversibel
necrosis
differece btw autolysis and necrosis=celldeaths
autoysis(lysososmes–>hydrolytic enzymes–>intracell material–>selfdigestion). IN DEAD BODY=POST MORETM CHNAGE AND NO INFLAMMATORY
necrosis: LIVING BODY, SURRONDED BY INFLAMMATORY CELLS
How does cell deth looks like
cytoplasm: homogenous, ^eosiniphilic(loss of rna and coagulation of proteins)
nucelar changes:
- pyknonsis: nucleus shrinkage–>darker and smaller
- karyorrhexis: frgamentation on nucleus
- karyolysis: diminishin of nucleus(loss of staining)
cellular details: lost but debris remains
ER:
- rER lose ribosmes
- may ubergo lyssi and drisupt
mitochondria:
- sweeling and leading to microgranular apperance of cytoplasm of cells
necrosis
intravital detah of cell, aka surroinding tissue is still alive
necrosis is the result of
liberation of intracellular enzymes following upon disruption of cytoplasmic organelles, disintegration of the nucelus and changes in the plasma membrane.
^conc of enzyems in blood
passage of ca2+ and na+ into cell, and K+ and enzymes out
liquefactive necrosis
- semiliquid (dissolution by hydrolytic enxymes)
- ^LIPID rich
- Only brain-arterial occlusion, bacterial ifnection
- cystic spaces
coagulative necrosis: divided into
caseous
fibrinoid
fat
haemorrhagic
gummatous
coagulation
- ^protein rich
- firm and pale
- still can see som archtectural
- caused by arterial occlusion
- HEART AND KIDNEY
COMES FORM PROTEIN DENATURATION
caseous necrosis
- cheese like, soft and white
- no architerctural (maybe some debris can be seen-like dusty)
- TUBERCULOSIS
gummatous
- 3rd stage of syphilis- spirochete bacteria(treponema pallidum)
- firm, rubbery, wollen, tender or painful
no architerture only pink with few nuclei - ## LIVER, SKIN, HEART, BRAIN, BONE , GENITALS
heamorrhagic necrosis
- dark and red
due to blackage of venous drainage of tissue–>congestion of blood (infarction of jejunum) or arterial failure of perfusion (lung infarcts)
fat necrosis
- fat by digestive enzymes: lipase releas FA from TAG–>FA + ca2+–>soaps–<white chalky deposits
- ACUTE PANCREATITIS (balzeri necrosis) OR TRAUMA TO PANCREAS, also brast, salivary glands neonates after traumatic delic\very
- foci of hard, yellow material
fibrinoid necrosis
- artieris in vasuculitis and hypertension
- deposition of fibrin like material
- acc of amorphous, basic proteinaceous material in tissue matrix
- pathologic immune complexe and autoimmune
what is gangrene
encrosis with superadded putrefication
- form coagualtive necrosso bc ischemia
- characterized primarly inflammation provoked by virulent bacterial
- is secondary form of necrosis
types of gangrene
dry: ischemia-distal part of limbs(toes)-buergers disease
wet:moist tissue like motuh, bowel, lung, cervic, vulva
gas: form of wet by gas forming clostridia
special forms of gangrnee
internal gangrene: affect multiple organs like intestines, gallbaldder, appendic
- blocked BF-liek twisting
- fever and pain
fourniers gangrene:
- genital organs
- men more
- in genital are or urinary tarct–>genitla pain, tenderness, redness, swellign
progressive bacterial synergistic gangerene(meleneys grangrene
- after operation–>skin lesions
noma: face
necrotzing fascitis: deep layers of skin
what is atrophy
simple decrease in cell size and number–>shrinkage of organs or tisse
pathologic but reversible
involution
atrphy of old age
- natural like thymus, uterus after gravidity, ovarian tissue
simple atrophy
decreae of cellualr size like hrart
numeric atrophy
decrease of cellular number like BM
causes of atrophy
gradual diminution of blood supply=low o2 and nutrients–>fall of cell activity and shrinkage
lipofusinc: undigestied lipid material
atrophy leads to
reduced functional activity(diffuse)
- atropgy of cells
- obstruction of galnd duct–>gland atorphy
interrupted nerve supply
- SM in poliomyelitis
endocrine deficiency
- loss of regualtiing mechnaism
- reduced metabolic act
- pituitary deficince–>thyroid, adrenal, gonads, genital organs atrophy
pressure
- interruption of blood supply and interference of funciton
- neoplasm pressing of surrounding tissyes
dystrophy is the
midlest form and ussually reverisible regressive chnages besides amyloidosis
protein dystrophies: types
albuminoid(parenchymatous), vacuolar = intracellular
hyaline and mucinous= both intracell and interstitial
fibrinoid and amyloid=interstitial
albuminoid/ parenchymal dystrophy
- mildest
- EX: kidney: pathological noxa–>mitochondria becomes enlarged–>granules
- cloudy swelling, by chabge of color of cytoplasm of cells,
-functional overload, hypoxia, ischmia
vacoluar dystrophy
- videre av alubminoid
- întake of water–>droplets/vacuoles=hydropic degenration
- tubular epo broken, see only fragments of cytoplasm
hyaline- intracellualr
- proteinaceous droplets within cells
- not true hyaline
- ex:
- russels bodies in plasma cells: acc immmunoglobulin
- mallory hyalin in hepatocytes: alcholism
- cells of procimal tubules in kidney
- cooks cells in adenohypofysis: cushings syndrome
- intracellular inclusions in viral infections (cytomegalovirus)
- hyaline dropletes in tumour cells (pheochromocytomatous)
-
epithelial hyaline
of prostate and cropora amylacea in prostate glands: COMMON FINDINF IN NODULAR PROSTATIC HYPERPLASIA
kidney: within tubules are accumulating proteins and this develops proteins cusps
hyalin dyrstrophy: interstitial
- degenerated collagen
- chronic inflammation: leads to fibrotisation , healing and scarring
- regressive chnges in tumours
hyaline: homogenoys apperanse, no cell elemets or vessels, eosinophilic amorphous apperance, similar to cartilage
mucin dystrophies: intarceulluar
- aka epithelial mucin, produces by goblet and mucinous glands
- quantitative and qualitative disorders in mucin production( hyper or hypocrinia), or qualitiy(dyscrinia)
- signet ring morphology: acc in cytoplasm
- extracellular accumulaiton of mucin in tumors
- ## cystic fibrosis (mucoviscoidosis)-dyscrinia
mucinous - interstitial
- mucopolysaccharides
- myxedema: hypofunction of TG-error of metabolism
- ganglion: near joints and tendons
- adenocardinomas
- signet cell apperance
- mucin stained with PAS
fibrinoid
mixture of fibrin, fibrinogen, circulating immunocomplexes and complement
fibrinoid sytrophies
- autoimmune and immunopathological disorder
- arterial hypertension: leaking of eaosinophilic, proteinaceous material to interstitum around vv
amyloidosis is always
irreverisble
what is amylodosis
disease caused by accumulation of pathological extracellular (interstitial) glycoprotein called amyloid(heterogenous group of proteins)
each type of amyloid has 2 components
Component P: identical for all types (5%)
- protein of blood plasma
Component F-fibrbillar: different -95
- amyloidogenic protein
-b pleated sheat
classification of amyloidosis
primary: AL type
- overproduction of immunoglobulin light chains
-b-cell lymphoma–>multiple myeloma
secondary: AA type
- produced after overproduction of protein of acute phase inflammation, aka serum amyloid protein
- long lasting chronic inflammation or some tumours
how does amyloid look like
eosinophilic, homogenous, amorphous material within interstitum
USE CONGO RED-
where can amyloid feposit
muscles, haert, kidney, git, liver, spkeen
lipid dyrstrophies- intracellular
steatosis:
- accuulation of lipids-TAG, in cytoplasm of cells of parenchymatous organs
- liver
- see multiple lipid droplets in hepatocytes
lipid dystrophies- interstitial
Free lipids in interstitium
- not extraceullar steaotis
- atherosclerosis
Lipomatosis:
- PROLIFERATION OF LIPOMATOUS TISSUE
- Find in adipocytes–>proliferating in interstitum
- in organs–>atrophy and volume of lost tissue replaced by lipomatous tissue=lipomatous atrophy
psudohyperthrophy: when we have enlarged organ but functional parenchyme is atrophic
mechanism of steatosis development
1) increased intake of lipid
- brain infarct: gligal cells pahgocytose necrotic tissue–>intake of tissue rich of lipif–>accumualiton–>foamy cells/lipophages
2) disroders of mobilization of lipids form cells
- poisings, drugs
- liver enzyme fucntion
3) disorders of intracellualr degradation of lipids
- lipidosis: disorders whrre we have inhertided defects in fucntion of enzymes
- GAUCHERS disease: acc in cells of mononuclear phagocyting systems
- affect apleen, liver, kidney, lungs, brain
4) increased synthesis of lipids
types of steatosis
- stetosis of sagnativa: îalimentary intake of lipids
- steatosis resoptive-brain infarction, cholesterolosis
- steatosis transportive-intoxification
4- statosis retentive-due to hypoxia(heart, liveR)
- due to venostasis
carbohydrate dystrophies
glycogen dystrophies
- metabolism
- only glycogen can be accumulated, not glucoseee
primary and secondary glycogen dystiophies
secondary: acc of gly in non-neoplastic and neoplastic tissues
primary: glycogenosis
1: von gierke (glu-6-phos)
2: pompe (lysosomal a1-6, a1-4 glucosidase
3: cori (a1-6 glucosidase
4: andersen (glycosyltransferase
5: mc ardle (muscular phosphorylase
6: hers (hepatal phosphoylase
7: thomson(muscular phosphofructokinase
Atrophia fusca is what and what does it affect
brown atrophy
- lipofuscin is stored in cells
-tissues are darker
- common IN LIVER AND MYOCARDIUM
- similar in accumulaiton of lipochrome in atrophic adipose tissue
Amyotrophia is caused by
Atrophy due from lack of usage, may be due to denervation atrophy.
- The basis is also in inactivity in peripheral nerve palsy
- Significant muscle atrophy occurs inpoliomyelitis, when the alpha motoneurons of the anterior horns of the spinal cord disappear (so-called amyotrophy = muscle denervation atrophy)
dysplastic changes include
increased number of mitoses, loss of cell polarity, nuclear pleomirphism
what grades are dysplaisa divided into
- Grade I - Mild / low: atypia involves < one - third
- Grade II - Moderate / intermediate: atypia involves one to two - thirds of the epithelial thickness
- Grade III - Severe / high: atypia involves > two - thirds of the epithelial thickness
what may we see in dysplasia
- Hyperkeratosis is the increased thickening of stratum corneum,
- Parakeratosis is Hyperkeratosis with retention of the nuclei in corneum,
- Acanthosis is Epidermal hyperplasia of the Stratum spinosum
what is gallmark of coagulative necrosis
hallmark of coagulative necrosis is conversion of normal cells into tombstones - outlines of the cells are retained so that the cell type can still be recognised but their cytoplasmic and nuclear details are lost.
