cell injury and cell death Flashcards
cellular responses to stress and injury includes:
1- adaptive repossess as:
- atrophy
- hypertrophy
- hyperplasia
2- reverssible cell injury
3- irreversible cell injury = cell death
- necrosis
- apoptosis
—– refers to the decrease in size or number pff cells due to loss of cell substance which leads to :
—- workload
—– of innervention
- aging , fetal development , inadequate nutrition
- atrophy
- decrease
- loss
—- refers to the increase in the cell size and it involves — activation protein synthesis and production of ——
occurs in :
- hypertrophy
- gene
- organelles
- occurs in cells incapable of division so no new cells just large cells , physiologic and skeletal muscle w excersise and pathologic left ventricular hypertrophy in hypertension
—– increase in number of cells and the size of the organ which occurs in organs capable of —- and is often associated with —-
its also physiologic and :
and pathologic as:
its a —- process but fertile soil for —-
- hyperplasia
- cellular divison
- hypertrophy
- hormonal as breast uterus during pregnancy and compensatory as partial hepatecomy
- pathologic as excessive hormonal and growth factor as thyroid and endometrial hyperplasia
- controlled process
- cancer
—– refers to the reversible change in which one adult cell type is replaced by another adult cell type and it can be a precursor for —-
metaplasia , cancer
genetic reprogramming of stem cells as:
- ciggerate smoking - respiratory epithelium -> squamous
- Barrett’s oesophagus - squamous epithelium —> intestinal epitheliam
are examples of —–
metaplasia
causes of cell injury :
1- — deprivation as: hypoxia and ischaemia which is the — in blood flow , shock
2- —- agents as trauma thermal injury and radiation
3- —- agents as posion , drugs , pollutants
4- —- agents
5- —– reactions
6- —- defects
7- —— deficiency or excess
- o2
- decrease
- physical
- chemical
- infectious
- immunological reactions
- genetic defects
- nutritional
mechanism of cellular injury :
1- cellular responses depends on the —- as:
2- consequence depends on the — as:
- injury as type severity and duration
- cell as type state and adaptability
mechanism of cellular injury : - cell systems most vulnerable to injuries are :
1- mitochondria for aerobic respiration and ate-sythesis
2- cell membrane
3- synthetic apparatus protein and enzymes
4- cytoskeleton
- genetic apparatus aka dna
mechanisms associated w injuries :
1-inhibition of —– which leads to atp depletionnn
2- —– damage
3- generation of —– species aka —-
4- defects in ——-
5- disruption of —–
6- damage to —
-aerobic respiration
- mitochondrial
- oxygen species as free radicals
- membrane permibilty aka membrane damage
- calcium homeostasis aka calcium influx
- dna and proteins
- increased anaerobic glycolysis
- reduced sodium pump = accumulation of sodium n water
- reduced calcium pump
- decreased atp
- decrease phosolipids
-nuclear chromatin damage - disruption of membrane and cytoskeletal proteins
are all mechanims for:
reversible injury due to decreased phosphorylation within the mitochondria
—- injury is when the mitochondria changes , extensive plasma membrane damage and injury to the lysosomal membrane which activates the enzymes and degrades damaged cells and the release of enzymes damage the surrounding cells
irreversible injury
—- highly unstable and reactive chemical species w a single unpaired electrons examples :
▪ Superoxide O2
▪ Hydrogen peroxide H2O2
▪ Hydroxyl ion OH-
free radicals
important:
the morphological changes associated w reversible injury:
- Cellular swelling (hydropic change, vacuolar
degeneration) - Ultra structural changes
▪ Plasma membrane alteration-blebbing
▪ Loss of microvilli
▪ Mitochondrial swelling
▪ Dilation of endoplasmic reticulum with detachment of
ribosomes
▪ Nuclear alterations
important:
morphological changes associated w irreversible injury:
Membrane damage:
▪ Plasma membrane → enzymes released (e.g.
troponin, amylase)
▪ Mitochondrial membrane
▪ Lysosome (lytic enzymes)
—- refers to the unplanned cell death
—- refers to the planned/programmed cell death in that is genetically controlled
- necrosis
- apoptosis
read:
necrosis and necrosis morphology
-Morphologic changes that follow cell death in a living tissue
-Death of a large group of cells
-It is due to a pathologic process (never physiologic)
-Enzymatic digestion of cell
▪ Autolysis
▪ Heterolysis
-Inflammation in the surrounding tissue
morphology :Cytoplasmic eosinophilia
Nuclear changes
▪ Pyknosis - condensation of the nucleus and clumping
of the chromatin (shrinking of nuclei)
▪ Karyorrhexis - fragmentation and breakdown of the
nucleus
▪ Karyolysis - pallor and dissolution
types of necrosis :
1-Coagulative necrosis: specific morphological pattern w preservation of structural outlines , hypoxic cell death except brain , cell shape and organ structures are preserved and the nuclei disappears
2-Liquefactive necrosis: transformation of solid tissue into a liquid mass and complete digestion of the dead cells , tissues are destroyed and enzymatic lysis of cells
3-Caseous necrosis: tuberculous infection , distinctive type of necrosis , cheesy crumbly and white gross appearance , granular debris surround by a ring pg gransloatous inflammation
4-Fat necrosis: necrosis of fat induced by lipase in pancreas or macrophages , fatty acids complex w ca++ to create calcium soap , fat trauma , fat necrosis in pancreatitis
5-Fibrinoid necrosis: necrotic damage to blood vessel wall and is associated w vasulatitis
6-Gangrenous necrosis: not a distinctive pattern of cell death , coagulative necrosis (mummified tissue - dry gangrene ) characteristic of ishaemia of lower limb , ishcemia w 2ndary bacterial infection ( liquefactive necrosis - wet gangrene ) , gas gangrene - clostridium infection
apoptosis refers to falling off and it involves — cells or — clusters and they have physiologic and pathologic processes ,its — dependent , —– is not induced , the cells will — and various genes regulate apoptosis as:
- single cell or small cluster
- energy
- inflammation
- shrink rapidly
- genes as:
▪ Anti-apoptotic: e.g. Bcl-2
▪ Pro-apoptotic: e.g. Bax
AIDS and nerodivegrentive diseases are associated with —–
Neoplasia and autoimmune disorders are associated w the increase of —-
- apoptosis
- cell survival
—– accumulation refers to the endogenous susbatane which is normal substance produced at normal or increase rate of metabolism inadquete for removal as fatty acids and lipofusin which is a pigment like a waste product rich in lipids
in this accumulation the normal or abnormal substances cant be metabolised which leads to storage diseases
while exogenous are the cells cant degrade substance as carbons and tattoos
intracellular accumulation
Abnormal deposition of calcium salts with smaller amounts of iron, magnesium and other mineral salts refers to —-
pathologic calcification and the 2 types are:
- dystrophic
- metastatic
—- refers to deposition of calcium in a necrotic tissue
▪ Normal serum calcium
▪ Areas of necrosis or injury
▪ Intracellular or extracellular
dystrophic calcification
—- refers to deposition of calcium in a normal tissue
▪ Occurs with hypercalcaemia
- Hyperparathyroidism, destruction of bone occurring
with tumours involving bone, vitamin D intoxication,
sarcoidosis, renal failure
▪ Occurs in normal tissue
▪ Primarily affects vessels, kidneys, lungs, and gastric
mucosa
metastatic calcification
the 2 theories of cellular aging:
1- —— refers to the accumulation of metabolic and genetic damage, free radical damage throughout life
2- —— cellular aging aka replicative senescence which include:
1- wear and tear
2- intransitive cellular aging
- predetermined genetic programming
- toleere shorting ( incomplete replication of chromosomes end which results in cell arrest )
