Cellular response to stress and noxious stimuli Flashcards
what are the properties of disease
- etiology (cause, risk factors)
- Pathogenesis
- Morphologic changes
- Clinical manifestations
what are the changes in response to physiological states (adaptations)
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
what is the increase in the size of cells which
increases the size of the organ
hypertrophy
what is an example of hypertrophy
fat gaining in adipose tissue (weight gain)
what causes
a) Physiologic hypertrophy
b) Pathologic hypertrophy
a) hormones, growth factors
b) work overload e.g. exercise
what are the mechanisms of hypertrophy
✓Increased production of cellular proteins
✓Switch of adult to fetal or neonatal forms
✓Re-expression of some shut down genes
what is hyperplasia
increment in the number of cells in an organ or tissue in response to a stimulus
true or false, hypertrophy and hyperplasia cannot occur at the same time
false they can
what kind of cells does hyperplasia only take place
in a tissue with cells capable of dividing i.e. not in muscle or nerve cells
what are the mechanisms of hyperplasia
✓Growth factor dependent proliferation of mature cells
✓Increased output of new cells from stem cells
what is the opposite of hypertrophy
atrophy (reduction in size of an organ or tissue due to a decrement in cell size & number)
where is physiological atrophy usually seen
in fetuses
what are the types of pathological atrophy
Disuse atrophy Denervation atrophy Senile atrophy Undernourishement Loss of endocrine stimulus Continuous pressure
what are the mechanisms of atrophy
- Nutrient deficiency or disuse
* autophagy (self-eating)
what are residual bodies
vesicles containing indigestible materials
what is example of residual bodies
Lipofuscin granules in brown atrophy
what is metaplasia
is a reversible change in which one differentiated cell type is replaced by another cell type which is better able to withstand the adverse environment
what are examples of metaplasia
✓Columnar epithelium → stratified squamous epithelium
✓Stratified squamous → mucinous epithelium
✓Connective tissue metaplasia
what are mechanisms of metaplasia
➢Reprogramming of stem cells
➢Reprogramming of mesenchymal cells in connective tissue
➢Cytokines, growth factors, extracellular matrix components causing gene expression and hence differentiation
➢Retinoic acid regulates progenitors derived from tissue stem cells
when does injury develop
- limits of adaptive responses are exceeded
- cells exposed to ınjurious agents, stress
- cells are deprived of essential nutrients
- compromised by mutations
what does reduction in oxidative phosporylation cause
→depleting energy stores (ATP)
→ ion pumps are affected then stop
→causing water influx
→ cells swell
what is hypoxia
Having low oxygen levels in your tissues
what can cause hypoxia
- Decreased blood flow (ischemia)
- Cardiorespiratory failure
- decreased oxygen carrying capacity of the blood
what can cause cell injury and death
oxygen deprivation physical agents chemical agents infectious agents immunologic response genetic derangements nutritional imbalance
what is the main change that occurs morphologically during reversible injury as seen on a light microscope
cellular swelling
what is vacuolar degeneration
cells show small clear vacuoles within the cytoplasm
what changes are seen on an electron microscope during reversible injury
▪Plasma membrane alterations; blebbing (protrusions of the cell membrane), blunting, loss of microvilli
▪Mitochondrial changes; swelling, small amorphous densities
▪Dilation of ER; detachement of polysomes, intracytoplasmic myelin figures
▪Nuclear alterations; disintegration of granular & fibrillary elements
what is it called when cells are lethally injured
necrosis
why do necrotic cells have a glassy homogenous appearance
because of loss of glycogen
why do myelin figures appear during cell necrosis
due to enzymes digesting the organelles and dead cell is replaced by whorled phospholipid structures called myelin figures
what forms in necrotic cells due to damaged membranes
calcium soaps causing calcification
define these three forms of changes in the nucleus
a) Karyolysis
b) Pyknosis
c) Karyorhexis
a) basophilia of the chromatin fades & DNA is dissolved
b) nucleus shrinks, basophilia increases, chromatin condenses into solid shrunken basophilic mass
c) pyknotic (irreversible condensation of chromatin) nucleus undergoes fragmentation
what are the types of necrosis
- coagulative necrosis
- liquefactive necrosis
- gangrenous necrosis
- caseous necrosis
- fat necrosis
- fibrinoid necrosis
what is the localized area of coagulative necrosis called
infarct
what happens to the architecture of dead tissues in coagulative necrosis
they are preserved
how are necrotic tissues removed in coagulative necrosis
by leucocytes
coagulative necrosis can affect everywhere except what organ
the brain
what leads to coagulative necrosis
obstructed vessels leading to ischemia (restriction in blood supply to tissues)
in coagulative necrosis how long does an anucleated cells persist
days or weeks
what process is blocked during coagulative necrosis and hence what does it stain
proteinolysis (due to enzyme denaturing) , eosinophilic
what does hypoxic death of cells within central nervous system often manifest as
liquefactive necrosis
what forms during liquefactive necrosis and why
pus forms because of tissue digestion
where does gangrenous necrosis usually occur
Seen usually in a limb which lost its blood supply
what happens when bacteria superimpose and turn to a liquefactive necrosis
wet gangrene
in which disease is caseous necrosis usually see
tuberculosis
what necrosis is usually associated with trauma to the pancreas
fat necrosis
how does fat saponification in fat necrosis occur
when fatty acid combines with calcium forming chalky deposits
what happens during fibrinoid necrosis
antigen antibody complexes deposit in the arterial walls causing fibrin deposition
what do does fibrinoid necrosis stain
bright eosinophilic
what does response to injurious stimuli depend on
the nature of the injury
its duration
severity
what causes hypoxia
Mechanical arterial obstruction
what restores blood flow to ischemic tissue and promotes recovery but paradoxically may exacerbate the injury causing cell death
Ischemia-reperfusion
what is a complement system
enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen’s cell membrane
what is toxic injury
conversion to toxic metabolites or direct toxicity
what is apoptosis
a tightly regulated suicide program within the cell
what are apoptotic bodies
fragments containing portions of nuclear & cytoplasmic material formed during apoptosis
what enzyme is mainly responsible for apoptosis
caspases
what are the mechanisms of apoptosis
- intrinsic pathway
2. extrinsic pathway
in the intrinsic pathway, what does cytochrome bind to in the cytosol
apoptosis activating factor1 forming an apoptosome which then binds to caspase-9 triggering a cascade of caspases
during intrinsic pathway what happens when the outer cell membrane becomes more permeable
release of death inducing pro-apoptotic molecules into the cytoplasm
what activates caspase 10 in the extrinsic pathway
Cytoplasmic domain intracellular apoptotic signals. the caspase 10 then activates caspase 8
what happens during execution phase
caspase system cleaves cytoplasmic DNAse inhibitor hence cleaving DNA and leading to dead cell removal
give 5 morphological changes during apoptosis
cell shrinkage
chromatin condensation
Formation of cytoplasmic blebs & apoptotic bodies
Phagocytosis of apoptotic cells by macrophages
Plasma membranes remain intact
which type of necrosis has no inflammation
apoptosis
what is another name for the extrinsic pathway
death receptor-initiated pathway of apoptosis
