Cell injury, degeneration and death Flashcards
Quick overview of causes of cell injury (similar to causes of disease).
- physical agents
- ______ _____
- _______
- ______ and ______
- ________ _____
- ______
- _____ _____
Quick overview of causes of cell injury (similar to causes of disease).
- physical agents
- chemical agents (+drugs)
- infections
- hypoxia and ischaemia
- immunological reactions
- nutrition
- genetic disorders
Cell injury can be _____ or ______.
______:
- changes due to environment stress
- return to normal once stimulus removed
_______:
- permanent
- cell death, usually necrosis, follow
Cell injury can be reversible or irreversible.
Reversible:
- changes due to environment stress
- return to normal once stimulus removed
Irreversible:
- permanent
- cell death, usually necrosis, follow
Cell injury pathogenesis (mechanisms) -
locations cells can be damaged:
- ______: disrupted aerobic respiration/ATP synthesis
- ___ _____: disrupted ion concentrations, esp increased Ca2+
- ______: includes _____, disrupted enzymes and structural proteins synthesis and architecture
- _____: disrupted DNA maintenance and DNA damage
Cell injury pathogenesis (mechanisms)
Damage to:
- mitochondria: disrupted aerobic respiration/ATP synthesis
- cell membrane: disrupted ion concentrations, esp increased Ca2+
- cytoplasm: includes ribosomes, so disrupted enzymes and structural proteins synthesis and architecture
- nucleus: disrupted DNA maintenance and DNA damage
Cell injury pathogenesis (mechanisms) - oxidative stress:
- oxidative stress caused by ______ _____ _____ (___ ____)
- normally in small amounts as byproducts of ______
- formed pathologically by _____, ___ _____, _____ etc
- lack of _______ makes damage more severe
Cell injury pathogenesis (mechanisms) - oxidative stress:
- oxidative stress caused by reactive oxygen species (free radicals)
- normally in small amounts as byproducts of respiration
- formed pathologically by radiation, toxic chemicals, hypoxia etc
- lack of antioxidants makes damage more severe
Changes are same whether reversible or irreversible, but reversible less severe.
Examples include:
- “____ ______” : osmotic distrubances with loss of energy-dependant Na pump causing high Na in cell
- “___ ____” : accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism, esp in liver
- “cytoplasmic blebs”
- “disrupted microvilli”
- “swollen mitochondria”
Pic for this in cell injury, degen and death folder.
Changes are same whether reversible or irreversible, but reversible less severe.
Examples include:
- “Cloudy swelling” : osmotic distrubances with loss of energy-dependant Na pump causing high Na in cell
- “Fatty change” : accumulation of lipid vacuoles in cytoplasm caused by disruption of fatty acid metabolism, esp in liver
- “cytoplasmic blebs” (like sacs of membrane containing cytoplasm hanging out of cell)
- “disrupted microvilli”
- “swollen mitochondria”
Pic for this in cell injury, degen and death folder.
After cell injury, death is usually by _____.
______ is uncontrolled and due to external stimuli, and always pathological.
______ is programmed / controlled, usually physiological. Can be pathological though, eg in a ____ ______.
Main difference between two is in _____ the ___ _____ ___ ___ whereas in _____ they do not.
After cell injury, death is usually by necrosis.
Necrosis is uncontrolled and due to external stimuli, and always pathological.
Apoptosis is programmed / controlled, usually physiological. Can be pathological though, eg in a viral infection.
Main difference between two is in necrosis the cell contents leak out whereas in apoptosis they do not.
_____ = necrosis caused by a loss of blood supply
Infarction
Histological changes in necrosis:
- ___ ______
- vacuolation
- disruption of _______ and organelles
- release of cell contents (enzymes released can cause ______ _____ and thus ___ ______)
- DNA disruption
Histological changes in necrosis:
- cell swelling
- vacuolation
- disruption of membrane and organelles
- release of cell contents (enzymes released can cause adjacent damage and thus acute inflammation)
- DNA disruption
Types of necrosis:
- _______ : firm, tissue maintained. Can be _______ (excess blood) due to venous blockage or ________ (lack of blood supply) which affects larger area.
- ________ : tissue becomes liquid and structure lost. Examples inc cerebral infarct, infective abscess.
- ______ : combination of _______ and _______, appears “cheese like”. Usually for granulomatous inflammation, esp TB in lung.
- ___ : due to action of lipases on ____ ____
Types of necrosis:
- Coagulative : firm, tissue maintained. Can be haemorrhagic (excess blood) due to venous blockage or gangrenous (lack of blood supply) which affects larger area.
- Colliquitive : tissue becomes liquid and structure lost. Examples inc cerebral infarct, infective abscess.
- Caseous : combination of coagulative and colliquitive, appears “cheese like”. Usually for granulomatous inflammation, esp TB in lung.
- Fat : due to action of lipases on fatty tissue
Necrosis causes release of cell contents which activates _______ and causes damage.
- Either ____ with removal of stimulus and then healing+repair
- Or _____ with persistence of stimulus (_____ ________).
Necrosis causes release of cell contents which activates inflammation and causes damage.
- Either acute with removal of stimulus and then healing+repair
- Or chronic with persistence of stimulus (chronic inflammation).
__________ apoptosis:
- __________, deletion of cell populations
- cell deletion in growing cell populations to maintain constant number eg epithelium
- deletion of inflammatory cells after immune response
- deletion of self-reactive _______ in the _____.
________ apoptosis:
- ____ ________, eg cytotoxic T-lymphocytes
- DNA damage
- hypoxia/ischaemia
Physiological apoptosis:
- embryogenesis, deletion of cell populations
- cell deletion in growing cell populations to maintain constant number eg epithelium
- deletion of inflammatory cells after immune response
- deletion of self-reactive lymphocytes in the thymus
Pathological apoptosis:
- viral infection, cytotoxic T-lymphocytes
- DNA damage
- hypoxia/ischaemia
Morphology of apoptosis:
- ___ _____
- _____ ______ (this is when nucleus is packaged up, does not happen in necrosis)
- stages of this^ can be found in pics folder
- __ ______ and _______ remain intact (unlike necrosis)
- _______ ___ form and break off to form apoptotic bodies which are _______ by _______.
Morphology of apoptosis:
- cell shrinkage
- chromatin condensation (this is when nucleus is packaged up, does not happen in necrosis)
- stages of this^ can be found in pics folder
- cell membrane and mitochondria remain intact (unlike necrosis)
- cytoplasmic blebs form and break off to form apoptotic bodies which are phagocytosed by macrophages.
_______ = abnormal accumulation of substances
Location may intracellular, extracellular or in connective tissue.
Composition:
- normal _______ substances (eg CHO/protein/lipid products of metabolism, pigments, mix of both)
- foreign _______ substances (eg pigments, industrial material)
Depositions = abnormal accumulation of substances
Location may intracellular, extracellular or in connective tissue.
Composition:
- normal endogenous substances (eg CHO/protein/lipid products of metabolism, pigments, mix of both)
- foreign exogenous substances (eg pigments, industrial material)
Deposition examples
Endogenous intracellular:
- ______
- _________
- lipid, inc cholesterol
also for endo intra,
- ‘storage disease’ eg alpha-1-antitrypsin in liver
- ‘degeneration products’ eg lipofuscin (a ‘wear-and-tear’ pigment)
Endogenous extracellular:
- ______
- _____
- calcium
Exogenous intracellular:
- _____ _______
- carbon (_______ - carbon in lungs)
- ______
Exogenous can be extracellular too.
Deposition examples
Endogenous intracellular:
- melanin
- haemosiderin
- lipid, inc cholesterol
Endogenous extracellular:
- amyloid
- fibrosis
- calcium
Exogenous intracellular:
- tattoo pigment
- carbon (anthracosis - carbon in lungs)
- asbestos
Exogenous can be extracellular too.
_____ = ____ protein fibrils form ______ aggregates, leads to accumulation of abnormal protein extracellularly. _____ is a pattern which can be produced by multiple proteins. Can be _____ or ______.
Occurs due to production of an ______ _____ or excessive production of a ____ _____.
Resembles fibrosis but without prior inflammation.
____ ___ stain is used as fibrils will stain pink.
Pics in folder.
Amyloid = soluble protein fibrils form insoluble aggregates, leads to accumulation of abnormal protein extracellularly. Amyloid is a pattern which can be produced by multiple proteins. Can be systemic or localised.
Occurs due to production of an abnormal protein or excessive production of a normal protein.
Resembles fibrosis but without prior inflammation.
Congo Red stain is used as fibrils will stain pink.
Pics in folder.
