cell damage and death Flashcards
(29 cards)
increased functional demand leads to?
hypertrophy= increase number of cells
hyperplasia= increase size of cells
decreased functional demand leads to
atrophy= decrease size of cells
hypoplasia= decrease number of cells
Goitre?
Thymus degeneration?
Uterus during pregnancy?
Lymphadenitis (enlargement of lymph node)?
Skeletal muscle?
Kidney (during renal artery stenosis)?
Goitre? HYPERPLASIA
Thymus degeneration? INVOLUTION (HYPOPLASIA)
Uterus during pregnancy? HYPERPLASIA
Lymphadenitis ? HYPERPLASIA
Skeletal muscle? HYPERTROPHY
Kidney (during renal artery stenosis)? ATROPHY
cell metaplasia?
change of 1 already matured / differentiated cell type to another
mechanisms of cell injury (4)
- cell membrane damage
- complement-mediated lysis via MAC - mitochondrial damage causing inadequate aerobic respiration
- hypoxia - ribosomal damage leading to altered protein synthesis
- alcohol in liver - nuclear damage
- virus
- radiation
-free radicals
(4) REVERSIBLE, EARLY STAGE changes when a cell undergoes stress.
cytoplasmic swelling
nucelar chromatin clumping
mitochondrial and ER swelling
fatty changes
(3) IRREVERSIBLE, LATE STAGE changes of a cell that’s about to undergo apoptosis.
nuclear condensation (shrinkage) (pyknosis)
nuclear disslution (karyolysis)
nucelar breakup (karyorrhexis)
Lysosomal rupture
Amorphous densities in mitochondrial matrix
fragmentation of cell membrane
what determines if a cell injury is reversible or irreversible?
- type of injury
- exposure time (duration of injury)
- severity of injury
cell stress response
- increase expression of protective proteins
- molecular chaperones (protect proteins from further damage)
- ubiquitin (remove damaged protein) - form aggregates of ubiquitin and damaged proteins (inclusion bodies)
eg Mallory’s hyaline bodies (alcoholic liver damage)
Lewy bodies (parkinson’s disease)
appear as dark circles within cells
autophagy
occurs in cell stress
autophagosomes eat own organelles -> atrophy
formation of residual bodies (vesicles containing indigestible materials) - accumulate as lipofuscin
impt of autophagy
- eliminate abnormal molecules (potentially toxic)
- recycle components of molecules (survival mechanism)
LATE STAGE APOPTOTIC cells stain more eosinophilic / basophilic?
eosinophilic (too much neutrophils which destroy materials like proteins)
- denatured proteins are eosinophilic
types of cell death
- autolysis (death of cells and tissues after death -> decomposition by post mortem release of digestive enzymes by lysosomes)
- apoptosis (programmed cell death)
- necrosis (death of cells in living tissues by breakdown of cell membrane
types of apoptosis
physiological -> regulate number of cells in tissue
- eg deletion of lymphocytes that are autoreactive
endometrial cells during menstruation
pathological
- eg hepatitis B, C virus induce hepatocytes to undergo apoptosis
eg HIV/AIDS -> CD4 helper t cells undergo apoptosis, causing decreased cell count and immunosuppression
process of apoptosis
physiological or pathological insult triggers cell to activate auto destructive enzymes
triggered enzymes cause changes in cell morphology (late stage changes) to form apoptotic bodies
through surface signals, apoptotic bodies engulfed by neighbouring normal cells/ macrophages
process of necrosis
release of hydrolytic enzymes from damaged lysosomes cause digestion and denaturation of cellular proteins and fragmentation of DNA
results in release of intracellular enzymes into extracellular space (good indicator of tissue damage)
initiation of inflammatory response
types of necrosis
coagulative necrosis
haemorrhagic necrosis
liquefactive necrosis
caseous necrosis
suppurative necrosis
necrosis vs apoptosis
number of cells
N: more cells, at tissue level
A: single cells
cell membrane
N: memb breaks down
A: memb intact
ATP:
N: passive -> no ATP because it is happening to the cell
A: active -> ATP because it is by the cell
inflammation
N: inflammatory
A: no inflammation
cause
N: ALWAYS patho
A: mostly physio, sometimes path
cellular aging
- decreased replication
- telomere shortening
- accumulation of damage
- DNA repair defects
- genetic and environmental insult
coagulative necrosis
- necrosis following hypoxia or ischemia
(reduced blood flow to tissue so less oxygen) - if necrosis following ischemia, infarction (blood flow to tissue cut so no oxygen)
- further from blood vessel, more prone to infarct
key feature: -ghost outline (cell membrane intact but no nucleus)
- necrosis is WHITE
hypoxia -> ischemia -> infarct -> necrosis
- most common necrosis and occurs in heart, liver, lungs
haemorrhagic necrosis
- necrosis in organs with dual blood supply or necrosis following venous congestion
(eg lung -> pulmonary artery and bronchial artery
liver -> hepatic artery and portal vein) - necrosis secondary to venous congestion -> obstruction of blood vessel -> rupture and ischaemia causing tissue death
- necrosis is RED
caseous necrosis
- necrosis following tuberculosis
- cheesy necrosis
key feature: granuloma (aggregates of epitheliod histiocytes)
- usually have Langhans Giant Cells (fused macrophages)
- granulomatous inflammation
- necrosis occurs at core of granuloma
- matter undergoing caseous necrosis histologically friable (crumbly)
liquefactive necrosis
- necrosis in brain following a stroke (cerebral infarction)
key feature: cystic “liquified” appearance (dissolution of dead tissue into liquid mass)
- fluid in liquefactive necrosis rich in fat (because neurons and glial cells very rich in fat)
suppurative necrosis
- necrosis with abscess formation
key feature: large collection of neutrophils
